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Huabio Inc anti elane antibody
Anti Elane Antibody, supplied by Huabio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+elane+antibody/anti+elane/10__1016_slash_j__apsb__2026__01__030-187-22-24
Average 86 stars, based on 1 article reviews
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Article Title: Engineered bacteria reprogram tumor microenvironment via cell senescence and neutrophil extracellular traps degradation
Article Snippet: For the detection of CitH3-DNA and NE-DNA, 96-well plates were coated overnight at 4 °C with anti-histone H3 antibody (Abcam, UK) or anti-ELANE antibody (Huabio, Hangzhou, China), respectively.



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Antibody sources and dilutions.
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Role <t>of</t> <t>MPO</t> and <t>ELANE</t> in the risk of alcohol-induced epilepsy risk. (A) The PPI network illustrates the overall interactions of overlapping genes. (B) The PPI network presents the top 8 hub genes among the overlapping genes. (C) Venn diagram showing the overlapping genes identified using the LASSO, RF, SVM-RFE, and PPI methods. (D) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (E) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure combined with chronic KA-induced epilepsy. n = 6; ∗∗∗∗ p < 0.0001. (F) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure in the PTZ-induced seizure model group compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (G) Schematic representation showing the experimental design. (H) Seizure latency in acute PTZ kindling model behavioral experiments. n = 7; ∗ p < 0.05. (I) Survival rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (J) Kindling rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (K) Proportion of mice with a Racine score of IV-V in the acute PTZ-kindling model. n = 7; ns, nonsignificant difference. Statistical significance was determined by Student's t -test (D–F, H) or the χ 2 test (I–K). Abbreviations: LASSO, least absolute shrinkage and selection operator; MPO, myeloperoxidase; RF, random forest; SVM-RFE, support vector machine-recursive feature elimination; PPI, protein–protein interaction.
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Role <t>of</t> <t>MPO</t> and <t>ELANE</t> in the risk of alcohol-induced epilepsy risk. (A) The PPI network illustrates the overall interactions of overlapping genes. (B) The PPI network presents the top 8 hub genes among the overlapping genes. (C) Venn diagram showing the overlapping genes identified using the LASSO, RF, SVM-RFE, and PPI methods. (D) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (E) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure combined with chronic KA-induced epilepsy. n = 6; ∗∗∗∗ p < 0.0001. (F) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure in the PTZ-induced seizure model group compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (G) Schematic representation showing the experimental design. (H) Seizure latency in acute PTZ kindling model behavioral experiments. n = 7; ∗ p < 0.05. (I) Survival rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (J) Kindling rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (K) Proportion of mice with a Racine score of IV-V in the acute PTZ-kindling model. n = 7; ns, nonsignificant difference. Statistical significance was determined by Student's t -test (D–F, H) or the χ 2 test (I–K). Abbreviations: LASSO, least absolute shrinkage and selection operator; MPO, myeloperoxidase; RF, random forest; SVM-RFE, support vector machine-recursive feature elimination; PPI, protein–protein interaction.
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TP receptor expression in DCs is negatively correlated with sepsis severity. a scRNA-seq analysis (SCP548) of immune cells in PBMCs from healthy controls ( n = 19) and patients with sepsis ( n = 29). b Percentages of immune cell populations in each cluster for both groups. c Correlation analysis between the percentage of DCs and the SOFA score in patients with sepsis ( n = 19 [control] and n = 29 [sepsis]). d scRNA-seq analysis of PG receptor expression in DCs from the PBMCs of healthy individuals. e Correlation analysis between TP receptor expression in DCs and SOFA score in sepsis patients ( n = 10 [control] and n = 24 [sepsis]). f Expression of TP in DCs from the PBMCs of controls and patients with sepsis ( n = 13 [control] and n = 24 [sepsis]). g Schematic representation of the sepsis model induced via lipopolysaccharide (LPS) and cecal ligation and puncture (CLP). h , i TP expression in primary DCs isolated from the spleens of LPS-treated and CLP-challenged mice ( n = 7–8 mice per group). j Survival curves of CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 28 mice per group). k , l Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs (n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 8 mice per group) and BALF protein levels ( o ) ( n = 8 mice per group) in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. p Quantitative analysis of <t>neutrophil</t> infiltration via measurement of MPO activity in lung tissue from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). q Representative histological images of lungs from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. Scale bars, 50 μm. r Quantification of the histology scores for lung injury in ( q ) ( n = 9 mice per group). Statistical significance was evaluated via Spearman’s correlation coefficient ( c , e ), Mann–Whitney U tests ( f , h , i , k – p , r ), or the log-rank test ( j )
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TP receptor expression in DCs is negatively correlated with sepsis severity. a scRNA-seq analysis (SCP548) of immune cells in PBMCs from healthy controls ( n = 19) and patients with sepsis ( n = 29). b Percentages of immune cell populations in each cluster for both groups. c Correlation analysis between the percentage of DCs and the SOFA score in patients with sepsis ( n = 19 [control] and n = 29 [sepsis]). d scRNA-seq analysis of PG receptor expression in DCs from the PBMCs of healthy individuals. e Correlation analysis between TP receptor expression in DCs and SOFA score in sepsis patients ( n = 10 [control] and n = 24 [sepsis]). f Expression of TP in DCs from the PBMCs of controls and patients with sepsis ( n = 13 [control] and n = 24 [sepsis]). g Schematic representation of the sepsis model induced via lipopolysaccharide (LPS) and cecal ligation and puncture (CLP). h , i TP expression in primary DCs isolated from the spleens of LPS-treated and CLP-challenged mice ( n = 7–8 mice per group). j Survival curves of CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 28 mice per group). k , l Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs (n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 8 mice per group) and BALF protein levels ( o ) ( n = 8 mice per group) in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. p Quantitative analysis of <t>neutrophil</t> infiltration via measurement of MPO activity in lung tissue from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). q Representative histological images of lungs from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. Scale bars, 50 μm. r Quantification of the histology scores for lung injury in ( q ) ( n = 9 mice per group). Statistical significance was evaluated via Spearman’s correlation coefficient ( c , e ), Mann–Whitney U tests ( f , h , i , k – p , r ), or the log-rank test ( j )
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TP receptor expression in DCs is negatively correlated with sepsis severity. a scRNA-seq analysis (SCP548) of immune cells in PBMCs from healthy controls ( n = 19) and patients with sepsis ( n = 29). b Percentages of immune cell populations in each cluster for both groups. c Correlation analysis between the percentage of DCs and the SOFA score in patients with sepsis ( n = 19 [control] and n = 29 [sepsis]). d scRNA-seq analysis of PG receptor expression in DCs from the PBMCs of healthy individuals. e Correlation analysis between TP receptor expression in DCs and SOFA score in sepsis patients ( n = 10 [control] and n = 24 [sepsis]). f Expression of TP in DCs from the PBMCs of controls and patients with sepsis ( n = 13 [control] and n = 24 [sepsis]). g Schematic representation of the sepsis model induced via lipopolysaccharide (LPS) and cecal ligation and puncture (CLP). h , i TP expression in primary DCs isolated from the spleens of LPS-treated and CLP-challenged mice ( n = 7–8 mice per group). j Survival curves of CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 28 mice per group). k , l Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs (n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 8 mice per group) and BALF protein levels ( o ) ( n = 8 mice per group) in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. p Quantitative analysis of <t>neutrophil</t> infiltration via measurement of MPO activity in lung tissue from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). q Representative histological images of lungs from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. Scale bars, 50 μm. r Quantification of the histology scores for lung injury in ( q ) ( n = 9 mice per group). Statistical significance was evaluated via Spearman’s correlation coefficient ( c , e ), Mann–Whitney U tests ( f , h , i , k – p , r ), or the log-rank test ( j )
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TP receptor expression in DCs is negatively correlated with sepsis severity. a scRNA-seq analysis (SCP548) of immune cells in PBMCs from healthy controls ( n = 19) and patients with sepsis ( n = 29). b Percentages of immune cell populations in each cluster for both groups. c Correlation analysis between the percentage of DCs and the SOFA score in patients with sepsis ( n = 19 [control] and n = 29 [sepsis]). d scRNA-seq analysis of PG receptor expression in DCs from the PBMCs of healthy individuals. e Correlation analysis between TP receptor expression in DCs and SOFA score in sepsis patients ( n = 10 [control] and n = 24 [sepsis]). f Expression of TP in DCs from the PBMCs of controls and patients with sepsis ( n = 13 [control] and n = 24 [sepsis]). g Schematic representation of the sepsis model induced via lipopolysaccharide (LPS) and cecal ligation and puncture (CLP). h , i TP expression in primary DCs isolated from the spleens of LPS-treated and CLP-challenged mice ( n = 7–8 mice per group). j Survival curves of CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 28 mice per group). k , l Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs (n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 8 mice per group) and BALF protein levels ( o ) ( n = 8 mice per group) in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. p Quantitative analysis of <t>neutrophil</t> infiltration via measurement of MPO activity in lung tissue from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). q Representative histological images of lungs from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. Scale bars, 50 μm. r Quantification of the histology scores for lung injury in ( q ) ( n = 9 mice per group). Statistical significance was evaluated via Spearman’s correlation coefficient ( c , e ), Mann–Whitney U tests ( f , h , i , k – p , r ), or the log-rank test ( j )
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Antibody sources and dilutions.

Journal: Cell Death & Disease

Article Title: NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury

doi: 10.1038/s41419-026-08995-5

Figure Lengend Snippet: Antibody sources and dilutions.

Article Snippet: Rabbit-anti-ELANE antibody , Abclonal , A8953 , 1:2000.

Techniques: Western Blot, Immunofluorescence

Role of MPO and ELANE in the risk of alcohol-induced epilepsy risk. (A) The PPI network illustrates the overall interactions of overlapping genes. (B) The PPI network presents the top 8 hub genes among the overlapping genes. (C) Venn diagram showing the overlapping genes identified using the LASSO, RF, SVM-RFE, and PPI methods. (D) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (E) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure combined with chronic KA-induced epilepsy. n = 6; ∗∗∗∗ p < 0.0001. (F) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure in the PTZ-induced seizure model group compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (G) Schematic representation showing the experimental design. (H) Seizure latency in acute PTZ kindling model behavioral experiments. n = 7; ∗ p < 0.05. (I) Survival rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (J) Kindling rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (K) Proportion of mice with a Racine score of IV-V in the acute PTZ-kindling model. n = 7; ns, nonsignificant difference. Statistical significance was determined by Student's t -test (D–F, H) or the χ 2 test (I–K). Abbreviations: LASSO, least absolute shrinkage and selection operator; MPO, myeloperoxidase; RF, random forest; SVM-RFE, support vector machine-recursive feature elimination; PPI, protein–protein interaction.

Journal: Genes & Diseases

Article Title: Multiomic insights into the MPO-mediated NET formation pathway in alcohol-induced epilepsy risk

doi: 10.1016/j.gendis.2025.101917

Figure Lengend Snippet: Role of MPO and ELANE in the risk of alcohol-induced epilepsy risk. (A) The PPI network illustrates the overall interactions of overlapping genes. (B) The PPI network presents the top 8 hub genes among the overlapping genes. (C) Venn diagram showing the overlapping genes identified using the LASSO, RF, SVM-RFE, and PPI methods. (D) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (E) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure combined with chronic KA-induced epilepsy. n = 6; ∗∗∗∗ p < 0.0001. (F) Representative immunoblots and quantification of MPO and ELANE protein expression in mouse hippocampal lysates after acute alcohol exposure in the PTZ-induced seizure model group compared with those in the control group. n = 6; ∗∗∗∗ p < 0.0001. (G) Schematic representation showing the experimental design. (H) Seizure latency in acute PTZ kindling model behavioral experiments. n = 7; ∗ p < 0.05. (I) Survival rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (J) Kindling rate in acute PTZ kindling model behavioral experiments. n = 7; ns, nonsignificant difference. (K) Proportion of mice with a Racine score of IV-V in the acute PTZ-kindling model. n = 7; ns, nonsignificant difference. Statistical significance was determined by Student's t -test (D–F, H) or the χ 2 test (I–K). Abbreviations: LASSO, least absolute shrinkage and selection operator; MPO, myeloperoxidase; RF, random forest; SVM-RFE, support vector machine-recursive feature elimination; PPI, protein–protein interaction.

Article Snippet: After 1 h of blocking with 5% skim milk in TBST at room temperature, the membranes were probed with primary antibodies, including those against GAPDH (Proteintech, 81640-5-RR), MPO (ABclonal, A24531), and ELANE (ABclonal, A13015), at 4 °C overnight.

Techniques: Western Blot, Expressing, Control, Selection, Plasmid Preparation

TP receptor expression in DCs is negatively correlated with sepsis severity. a scRNA-seq analysis (SCP548) of immune cells in PBMCs from healthy controls ( n = 19) and patients with sepsis ( n = 29). b Percentages of immune cell populations in each cluster for both groups. c Correlation analysis between the percentage of DCs and the SOFA score in patients with sepsis ( n = 19 [control] and n = 29 [sepsis]). d scRNA-seq analysis of PG receptor expression in DCs from the PBMCs of healthy individuals. e Correlation analysis between TP receptor expression in DCs and SOFA score in sepsis patients ( n = 10 [control] and n = 24 [sepsis]). f Expression of TP in DCs from the PBMCs of controls and patients with sepsis ( n = 13 [control] and n = 24 [sepsis]). g Schematic representation of the sepsis model induced via lipopolysaccharide (LPS) and cecal ligation and puncture (CLP). h , i TP expression in primary DCs isolated from the spleens of LPS-treated and CLP-challenged mice ( n = 7–8 mice per group). j Survival curves of CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 28 mice per group). k , l Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs (n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 8 mice per group) and BALF protein levels ( o ) ( n = 8 mice per group) in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. p Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). q Representative histological images of lungs from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. Scale bars, 50 μm. r Quantification of the histology scores for lung injury in ( q ) ( n = 9 mice per group). Statistical significance was evaluated via Spearman’s correlation coefficient ( c , e ), Mann–Whitney U tests ( f , h , i , k – p , r ), or the log-rank test ( j )

Journal: Signal Transduction and Targeted Therapy

Article Title: Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment

doi: 10.1038/s41392-026-02592-w

Figure Lengend Snippet: TP receptor expression in DCs is negatively correlated with sepsis severity. a scRNA-seq analysis (SCP548) of immune cells in PBMCs from healthy controls ( n = 19) and patients with sepsis ( n = 29). b Percentages of immune cell populations in each cluster for both groups. c Correlation analysis between the percentage of DCs and the SOFA score in patients with sepsis ( n = 19 [control] and n = 29 [sepsis]). d scRNA-seq analysis of PG receptor expression in DCs from the PBMCs of healthy individuals. e Correlation analysis between TP receptor expression in DCs and SOFA score in sepsis patients ( n = 10 [control] and n = 24 [sepsis]). f Expression of TP in DCs from the PBMCs of controls and patients with sepsis ( n = 13 [control] and n = 24 [sepsis]). g Schematic representation of the sepsis model induced via lipopolysaccharide (LPS) and cecal ligation and puncture (CLP). h , i TP expression in primary DCs isolated from the spleens of LPS-treated and CLP-challenged mice ( n = 7–8 mice per group). j Survival curves of CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 28 mice per group). k , l Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs (n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 8 mice per group) and BALF protein levels ( o ) ( n = 8 mice per group) in CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. p Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs ( n = 6 mice per group). q Representative histological images of lungs from CLP-challenged mice after adoptive transfer of WT DCs or TP −/− DCs. Scale bars, 50 μm. r Quantification of the histology scores for lung injury in ( q ) ( n = 9 mice per group). Statistical significance was evaluated via Spearman’s correlation coefficient ( c , e ), Mann–Whitney U tests ( f , h , i , k – p , r ), or the log-rank test ( j )

Article Snippet: After incubation with 5% bovine saline albumin in PBS for 30 min, the samples were incubated with primary antibodies against Ly6G/Ly6C (Invitrogen, Cat# 14-5931-82) and neutrophil elastase (ABclonal, Cat# A13015) for 12 h at 4 °C, followed by washing with PBS and incubation with Alexa Fluor 594- (Invitrogen, Cat# A-21207) or Alexa Fluor 488- (Invitrogen, Cat# A11008) for 2 h in the dark at room temperature.

Techniques: Expressing, Control, Ligation, Isolation, Adoptive Transfer Assay, Clinical Proteomics, Permeability, Activity Assay, MANN-WHITNEY

TP ablation in DCs exacerbates CLP- and LPS-induced sepsis in mice. a Survival analysis of CLP-challenged TP flox/flox ( n = 20 mice) and TP flox/flox CD11c Cre ( n = 27 mice) mice. b , c Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice ( n = 8 mice per group). d Lung vascular permeability detected by EBD leakage in TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP ( n = 6 mice per group). Lung wet/dry weight ratio ( e ) ( n = 6–8 mice per group) and BALF protein levels ( f ) ( n = 6–8 mice per group) in lungs from TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP. g Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP ( n = 6 mice per group). h Representative histological images of lungs from CLP-challenged (0, 1, and 3 days) TP flox/flox and TP flox/flox CD11c Cre mice. Scale bars, 50 μm. i Quantification of histology scores for lung injury in ( h ) (n = 6–9 mice per group). j Survival analysis of LPS-treated TP flox/flox ( n = 15 mice) and TP flox/flox CD11c Cre ( n = 15 mice) mice. k , l Plasma cytokine levels of proinflammatory (IL-1β) and anti-inflammatory (IL-10) markers in LPS-treated TP flox/flox and TP flox/flox CD11c Cre mice ( n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in LPS-treated (0, 8, and 24 h) TP flox/flox and TP flox/flox CD11c Cre mice ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 6 mice per group) and BALF protein levels ( o ) ( n = 5–6 mice per group) in LPS-treated (0, 8, and 24 h) TP flox/flox and TP flox/flox CD11c Cre mice. p Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from LPS-treated (0, 8, and 24 h) TP flox/flox and TP flox/flox CD11c Cre mice ( n = 6 mice per group). q Histological analysis of lung sections from LPS-treated (0, 8, and 24 hours) TP flox/flox and TP flox/flox CD11c Cre mice. Scale bars, 50 μm. r Lung histological scores corresponding to ( q ) ( n = 4 mice at 0 h, 6–8 mice at 8 and 24 h). Statistical significance was evaluated via two-way ANOVA followed by Sidak’s test for multiple comparisons ( b ‒ g , i , k ‒ p , r ) or the log-rank test ( a and j )

Journal: Signal Transduction and Targeted Therapy

Article Title: Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment

doi: 10.1038/s41392-026-02592-w

Figure Lengend Snippet: TP ablation in DCs exacerbates CLP- and LPS-induced sepsis in mice. a Survival analysis of CLP-challenged TP flox/flox ( n = 20 mice) and TP flox/flox CD11c Cre ( n = 27 mice) mice. b , c Plasma concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice ( n = 8 mice per group). d Lung vascular permeability detected by EBD leakage in TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP ( n = 6 mice per group). Lung wet/dry weight ratio ( e ) ( n = 6–8 mice per group) and BALF protein levels ( f ) ( n = 6–8 mice per group) in lungs from TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP. g Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP ( n = 6 mice per group). h Representative histological images of lungs from CLP-challenged (0, 1, and 3 days) TP flox/flox and TP flox/flox CD11c Cre mice. Scale bars, 50 μm. i Quantification of histology scores for lung injury in ( h ) (n = 6–9 mice per group). j Survival analysis of LPS-treated TP flox/flox ( n = 15 mice) and TP flox/flox CD11c Cre ( n = 15 mice) mice. k , l Plasma cytokine levels of proinflammatory (IL-1β) and anti-inflammatory (IL-10) markers in LPS-treated TP flox/flox and TP flox/flox CD11c Cre mice ( n = 8 mice per group). m Lung vascular permeability detected by EBD leakage in LPS-treated (0, 8, and 24 h) TP flox/flox and TP flox/flox CD11c Cre mice ( n = 6 mice per group). Lung wet/dry weight ratio ( n ) ( n = 6 mice per group) and BALF protein levels ( o ) ( n = 5–6 mice per group) in LPS-treated (0, 8, and 24 h) TP flox/flox and TP flox/flox CD11c Cre mice. p Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from LPS-treated (0, 8, and 24 h) TP flox/flox and TP flox/flox CD11c Cre mice ( n = 6 mice per group). q Histological analysis of lung sections from LPS-treated (0, 8, and 24 hours) TP flox/flox and TP flox/flox CD11c Cre mice. Scale bars, 50 μm. r Lung histological scores corresponding to ( q ) ( n = 4 mice at 0 h, 6–8 mice at 8 and 24 h). Statistical significance was evaluated via two-way ANOVA followed by Sidak’s test for multiple comparisons ( b ‒ g , i , k ‒ p , r ) or the log-rank test ( a and j )

Article Snippet: After incubation with 5% bovine saline albumin in PBS for 30 min, the samples were incubated with primary antibodies against Ly6G/Ly6C (Invitrogen, Cat# 14-5931-82) and neutrophil elastase (ABclonal, Cat# A13015) for 12 h at 4 °C, followed by washing with PBS and incubation with Alexa Fluor 594- (Invitrogen, Cat# A-21207) or Alexa Fluor 488- (Invitrogen, Cat# A11008) for 2 h in the dark at room temperature.

Techniques: Clinical Proteomics, Permeability, Activity Assay

TP deficiency enhances neutrophil recruitment by increasing S100a8/a9 expression. a scRNA-seq analysis of CD45 + immune cells isolated from the spleens of TP flox/flox and TP flox/flox CD11c Cre ( n = 2 mice per group) mice at 3 days post-CLP. b Dot plots showing the expression level of the canonical annotation marker used for cluster annotation. c Proportions of immune cell clusters in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice. Percentages ( d ) and numbers ( e ) of neutrophils (CD45 + CD3 − Ly6G + ) in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP. ( n = 4–6 mice per group). f Schematic of the neutrophil transwell migration assay. CFSE-labeled neutrophils from bone marrow were placed in the upper chamber, whereas DCs from TP flox/flox or TP flox/flox CD11c Cre mice were seeded in the lower chamber. Neutrophil migration was assessed after 2 h (Created with BioRender.com). g Quantification of neutrophil migration toward DCs from TP flox/flox and TP flox/flox CD11c Cre mice at 0 and 3 days post-CLP. ( n = 6 mice per group). h The correlation between TP receptor expression in blood DCs and neutrophil percentages in patients with sepsis ( n = 12 [control] and n = 23 [sepsis]) was analyzed. i Volcano plot of differentially expressed genes in DCs between TP flox/flox and TP flox/flox CD11c Cre mice (p.adjust < 0.05, Log2FC ≥ 0.5). j Top 10 enriched GO pathways associated with DEGs in TP flox/flox CD11c Cre vs TP flox/flox DCs. The mRNA expression of S100a8 ( k ) and S100a9 ( l ) in primary DCs from the spleens of CLP-challenged mice ( n = 4–6 mice per group). Plasma concentrations of S100a8 ( m ) and S100a9 ( n ) in CLP-treated (0 and 3 days) TP flox/flox and TP flox/flox CD11c Cre mice ( n = 8 mice per group). o , p Correlation analysis between TP and S100A8/A9 expression in blood DCs from patients with sepsis ( n = 12 [control] and n = 17 [sepsis]). q Neutrophil migration assay using DCs from TP flox/flox and TP flox/flox CD11c Cre mice post-CLP (3 days), with or without paquinimod ( n = 6–9 mice per group). r Schematic illustration showing that the deletion of TP promotes DC-mediated neutrophil recruitment through increased S100a8/a9 expression (Created with BioRender.com). Statistical significance was evaluated via Spearman’s correlation coefficient ( h , o , p ) and two-way ANOVA, followed by Sidak’s test ( d , e ) or Tukey’s test ( g , k – n , q ) for multiple comparisons

Journal: Signal Transduction and Targeted Therapy

Article Title: Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment

doi: 10.1038/s41392-026-02592-w

Figure Lengend Snippet: TP deficiency enhances neutrophil recruitment by increasing S100a8/a9 expression. a scRNA-seq analysis of CD45 + immune cells isolated from the spleens of TP flox/flox and TP flox/flox CD11c Cre ( n = 2 mice per group) mice at 3 days post-CLP. b Dot plots showing the expression level of the canonical annotation marker used for cluster annotation. c Proportions of immune cell clusters in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice. Percentages ( d ) and numbers ( e ) of neutrophils (CD45 + CD3 − Ly6G + ) in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice at 0, 1, and 3 days post-CLP. ( n = 4–6 mice per group). f Schematic of the neutrophil transwell migration assay. CFSE-labeled neutrophils from bone marrow were placed in the upper chamber, whereas DCs from TP flox/flox or TP flox/flox CD11c Cre mice were seeded in the lower chamber. Neutrophil migration was assessed after 2 h (Created with BioRender.com). g Quantification of neutrophil migration toward DCs from TP flox/flox and TP flox/flox CD11c Cre mice at 0 and 3 days post-CLP. ( n = 6 mice per group). h The correlation between TP receptor expression in blood DCs and neutrophil percentages in patients with sepsis ( n = 12 [control] and n = 23 [sepsis]) was analyzed. i Volcano plot of differentially expressed genes in DCs between TP flox/flox and TP flox/flox CD11c Cre mice (p.adjust < 0.05, Log2FC ≥ 0.5). j Top 10 enriched GO pathways associated with DEGs in TP flox/flox CD11c Cre vs TP flox/flox DCs. The mRNA expression of S100a8 ( k ) and S100a9 ( l ) in primary DCs from the spleens of CLP-challenged mice ( n = 4–6 mice per group). Plasma concentrations of S100a8 ( m ) and S100a9 ( n ) in CLP-treated (0 and 3 days) TP flox/flox and TP flox/flox CD11c Cre mice ( n = 8 mice per group). o , p Correlation analysis between TP and S100A8/A9 expression in blood DCs from patients with sepsis ( n = 12 [control] and n = 17 [sepsis]). q Neutrophil migration assay using DCs from TP flox/flox and TP flox/flox CD11c Cre mice post-CLP (3 days), with or without paquinimod ( n = 6–9 mice per group). r Schematic illustration showing that the deletion of TP promotes DC-mediated neutrophil recruitment through increased S100a8/a9 expression (Created with BioRender.com). Statistical significance was evaluated via Spearman’s correlation coefficient ( h , o , p ) and two-way ANOVA, followed by Sidak’s test ( d , e ) or Tukey’s test ( g , k – n , q ) for multiple comparisons

Article Snippet: After incubation with 5% bovine saline albumin in PBS for 30 min, the samples were incubated with primary antibodies against Ly6G/Ly6C (Invitrogen, Cat# 14-5931-82) and neutrophil elastase (ABclonal, Cat# A13015) for 12 h at 4 °C, followed by washing with PBS and incubation with Alexa Fluor 594- (Invitrogen, Cat# A-21207) or Alexa Fluor 488- (Invitrogen, Cat# A11008) for 2 h in the dark at room temperature.

Techniques: Expressing, Isolation, Marker, Transwell Migration Assay, Labeling, Migration, Control, Clinical Proteomics

Deletion of S100a9 in DCs alleviates CLP-induced sepsis in mice. a Survival analysis of CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 20–26 mice per group). b , c Plasma cytokine levels of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 8 mice per group). d Representative flow plots showing the percentages of DCs in the spleens of CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Quantification of DC percentages ( e ) and absolute numbers ( f ) in the spleens of CLP-challenged mice from ( d ) ( n = 6–8 mice). g Representative flow plots showing the percentages of neutrophils in the spleens of CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Quantification of neutrophil percentages ( h ) and absolute numbers ( i ) in the spleens of CLP-challenged mice from ( g ) ( n = 6–8 mice). j Representative immunofluorescence images showing the expression of neutrophil elastase (NE) and Ly6G in lung sections from CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Scale bars, 50 and 25 μm. k Quantification of NE-positive neutrophils in the lungs of ( j ) (n = 7–8 mice per group). l Western blot analysis of citH3 (NET marker) in the lungs of CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice after CLP challenge. m Quantification of protein levels in ( l ) ( n = 7 per group). n Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 6 mice per group). o Lung vascular permeability detected by EBD leakage in CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 6 mice per group). Lung wet/dry weight ratio ( p ) (n = 8 mice per group) and BALF protein levels ( q ) ( n = 8 mice per group) in CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. r Representative histology images of lung tissue from CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Scale bars, 50 μm. s Lung histology scores from ( r ) ( n = 7–9 mice per group). t Schematic illustration showing that ablation of S100a9 abolishes the enhanced neutrophil recruitment driven by TP-deficient DCs (Created with BioRender.com). Statistical significance was evaluated by one-way ANOVA followed by Tukey’s test for multiple comparisons ( b , c , e , f , h , i , k , m – q , s ) or the log-rank test ( a )

Journal: Signal Transduction and Targeted Therapy

Article Title: Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment

doi: 10.1038/s41392-026-02592-w

Figure Lengend Snippet: Deletion of S100a9 in DCs alleviates CLP-induced sepsis in mice. a Survival analysis of CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 20–26 mice per group). b , c Plasma cytokine levels of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 8 mice per group). d Representative flow plots showing the percentages of DCs in the spleens of CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Quantification of DC percentages ( e ) and absolute numbers ( f ) in the spleens of CLP-challenged mice from ( d ) ( n = 6–8 mice). g Representative flow plots showing the percentages of neutrophils in the spleens of CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Quantification of neutrophil percentages ( h ) and absolute numbers ( i ) in the spleens of CLP-challenged mice from ( g ) ( n = 6–8 mice). j Representative immunofluorescence images showing the expression of neutrophil elastase (NE) and Ly6G in lung sections from CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Scale bars, 50 and 25 μm. k Quantification of NE-positive neutrophils in the lungs of ( j ) (n = 7–8 mice per group). l Western blot analysis of citH3 (NET marker) in the lungs of CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice after CLP challenge. m Quantification of protein levels in ( l ) ( n = 7 per group). n Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 6 mice per group). o Lung vascular permeability detected by EBD leakage in CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice ( n = 6 mice per group). Lung wet/dry weight ratio ( p ) (n = 8 mice per group) and BALF protein levels ( q ) ( n = 8 mice per group) in CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. r Representative histology images of lung tissue from CLP-challenged CD11c Cre , TP flox/flox CD11c Cre , S100a9 flox/flox CD11c Cre , and TP flox/flox S100a9 flox/flox CD11c Cre mice. Scale bars, 50 μm. s Lung histology scores from ( r ) ( n = 7–9 mice per group). t Schematic illustration showing that ablation of S100a9 abolishes the enhanced neutrophil recruitment driven by TP-deficient DCs (Created with BioRender.com). Statistical significance was evaluated by one-way ANOVA followed by Tukey’s test for multiple comparisons ( b , c , e , f , h , i , k , m – q , s ) or the log-rank test ( a )

Article Snippet: After incubation with 5% bovine saline albumin in PBS for 30 min, the samples were incubated with primary antibodies against Ly6G/Ly6C (Invitrogen, Cat# 14-5931-82) and neutrophil elastase (ABclonal, Cat# A13015) for 12 h at 4 °C, followed by washing with PBS and incubation with Alexa Fluor 594- (Invitrogen, Cat# A-21207) or Alexa Fluor 488- (Invitrogen, Cat# A11008) for 2 h in the dark at room temperature.

Techniques: Clinical Proteomics, Immunofluorescence, Expressing, Western Blot, Marker, Activity Assay, Permeability

Blocking the S100a8/a9 receptor (TLR4) alleviated sepsis. a Survival analysis of CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment ( n = 21–26 mice per group). b , c Plasma cytokine levels of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment ( n = 8 mice per group). d Representative flow plots showing the percentages of DCs in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment following CLP challenge. Quantification of the percentages ( e ) and absolute numbers ( f ) of splenic DCs in ( d ) ( n = 7–8 mice per group). g Representative flow plots showing the percentages of neutrophils in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment following CLP challenge. Quantification of splenic neutrophil percentages ( h ) and numbers ( i ) in ( g ) (n = 6–8 mice per group). j Representative immunofluorescence images showing the expression of NE and Ly6G in lung sections from CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment. Scale bars, 50 and 25 μm. k Quantification of NE-positive neutrophils in the lungs of ( j ) ( n = 6–8 mice per group). l Western blot analysis of citH3 in the lungs of TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment after CLP challenge. m Quantification of protein levels in ( l ) ( n = 7 mice per group). n Representative histology images of lung tissues from CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment. Scale bars, 50 μm. o Lung injury score quantification based on histological evaluation of the data in ( n ) ( n = 4–6 mice per group). Lung wet/dry weight ratio ( p ) and BALF protein levels ( q ) in CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment ( n = 8 mice per group). r Schematic illustration showing that blockade of the S100a8/a9 receptor TLR4 negates the increased neutrophil recruitment induced by TP-deficient DCs (Created with BioRender.com). Statistical significance was evaluated via two-way ANOVA followed by Tukey’s test for multiple comparisons ( b , c , e , f , h , i , k , m , o – q ) or the log-rank test ( a )

Journal: Signal Transduction and Targeted Therapy

Article Title: Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment

doi: 10.1038/s41392-026-02592-w

Figure Lengend Snippet: Blocking the S100a8/a9 receptor (TLR4) alleviated sepsis. a Survival analysis of CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment ( n = 21–26 mice per group). b , c Plasma cytokine levels of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment ( n = 8 mice per group). d Representative flow plots showing the percentages of DCs in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment following CLP challenge. Quantification of the percentages ( e ) and absolute numbers ( f ) of splenic DCs in ( d ) ( n = 7–8 mice per group). g Representative flow plots showing the percentages of neutrophils in the spleens of TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment following CLP challenge. Quantification of splenic neutrophil percentages ( h ) and numbers ( i ) in ( g ) (n = 6–8 mice per group). j Representative immunofluorescence images showing the expression of NE and Ly6G in lung sections from CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment. Scale bars, 50 and 25 μm. k Quantification of NE-positive neutrophils in the lungs of ( j ) ( n = 6–8 mice per group). l Western blot analysis of citH3 in the lungs of TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment after CLP challenge. m Quantification of protein levels in ( l ) ( n = 7 mice per group). n Representative histology images of lung tissues from CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment. Scale bars, 50 μm. o Lung injury score quantification based on histological evaluation of the data in ( n ) ( n = 4–6 mice per group). Lung wet/dry weight ratio ( p ) and BALF protein levels ( q ) in CLP-challenged TP flox/flox and TP flox/flox CD11c Cre mice with or without Resatorvid treatment ( n = 8 mice per group). r Schematic illustration showing that blockade of the S100a8/a9 receptor TLR4 negates the increased neutrophil recruitment induced by TP-deficient DCs (Created with BioRender.com). Statistical significance was evaluated via two-way ANOVA followed by Tukey’s test for multiple comparisons ( b , c , e , f , h , i , k , m , o – q ) or the log-rank test ( a )

Article Snippet: After incubation with 5% bovine saline albumin in PBS for 30 min, the samples were incubated with primary antibodies against Ly6G/Ly6C (Invitrogen, Cat# 14-5931-82) and neutrophil elastase (ABclonal, Cat# A13015) for 12 h at 4 °C, followed by washing with PBS and incubation with Alexa Fluor 594- (Invitrogen, Cat# A-21207) or Alexa Fluor 488- (Invitrogen, Cat# A11008) for 2 h in the dark at room temperature.

Techniques: Blocking Assay, Clinical Proteomics, Immunofluorescence, Expressing, Western Blot

Specific activation of TP in DCs attenuates CLP-induced sepsis in mice. a Schematic illustration of the synthesis of DCpep-U-46619 (Created with BioRender.com). b Schematic illustration of the experimental design of DCpep-U-46619 treatment in CLP-induced sepsis. c Representative flow plots of spleen DCs and non-DC cells from mice treated with or without DCpep-U-46619. d Quantification of the percentages of DCpep-labeled DCs and non-DC cells from mice treated with or without DCpep-U-46619 ( c ) ( n = 3–5 mice per group). e Survival analysis of CLP-challenged wild-type (WT) mice following treatment with DCpep-U-46619 ( n = 20–24 mice per group). f , g Plasma cytokine concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged WT mice receiving PBS, DCpep, U-46619, or DCpep-U-46619 treatment ( n = 8 mice per group). h Representative flow plots showing the percentages of DCs in the spleens of CLP-challenged WT mice subjected to different treatments. Quantification of the percentages ( i ) and absolute numbers ( j ) of spleen DCs in the mice from ( h ) ( n = 5–7 mice per group). k Representative flow plots showing the percentages of neutrophils in the spleens of CLP-challenged WT mice subjected to different treatments. Quantification of the percentages ( l ) and absolute numbers ( m ) of splenic neutrophils in the mice in ( k ) ( n = 4–6 mice per group). n Representative immunofluorescence images showing the expression of NE and Ly6G in lung sections from CLP-challenged WT mice subjected to different treatments. Scale bars, 50 and 25 μm. o Quantification of NE-positive neutrophils in the lungs of ( n ) ( n = 6–7 mice per group). p Western blot analysis of citH3 in the lungs of CLP-challenged WT mice subjected to different treatments. q Quantification of protein levels in ( p ) ( n = 6–7 per group). r Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from CLP-challenged WT mice subjected to different treatments ( n = 6 mice per group). s Lung vascular permeability detected by EBD leakage in CLP-challenged WT mice subjected to different treatments ( n = 6 mice per group). Lung wet/dry weight ratio ( t ) ( n = 6 mice per group) and BALF protein levels ( u ) ( n = 6 mice per group) in CLP-challenged WT mice subjected to different treatments. v Representative histological images of lungs from CLP-challenged WT mice subjected to different treatments. Scale bars, 50 μm. w Quantification of lung injury scores on the basis of histological images from (v) ( n = 4–6 mice per group). Statistical significance was evaluated via one-way ANOVA followed by Tukey’s test for multiple comparisons ( f , g , i , j , l , m , o , q – u , w ) or two-way ANOVA followed by Tukey’s test for multiple comparisons ( d ) and the log-rank test ( e )

Journal: Signal Transduction and Targeted Therapy

Article Title: Thromboxane receptor activation in dendritic cells mitigates sepsis by suppressing S100a8/a9-mediated neutrophil recruitment

doi: 10.1038/s41392-026-02592-w

Figure Lengend Snippet: Specific activation of TP in DCs attenuates CLP-induced sepsis in mice. a Schematic illustration of the synthesis of DCpep-U-46619 (Created with BioRender.com). b Schematic illustration of the experimental design of DCpep-U-46619 treatment in CLP-induced sepsis. c Representative flow plots of spleen DCs and non-DC cells from mice treated with or without DCpep-U-46619. d Quantification of the percentages of DCpep-labeled DCs and non-DC cells from mice treated with or without DCpep-U-46619 ( c ) ( n = 3–5 mice per group). e Survival analysis of CLP-challenged wild-type (WT) mice following treatment with DCpep-U-46619 ( n = 20–24 mice per group). f , g Plasma cytokine concentrations of proinflammatory (IL-1β) and anti-inflammatory (IL-10) cytokines in CLP-challenged WT mice receiving PBS, DCpep, U-46619, or DCpep-U-46619 treatment ( n = 8 mice per group). h Representative flow plots showing the percentages of DCs in the spleens of CLP-challenged WT mice subjected to different treatments. Quantification of the percentages ( i ) and absolute numbers ( j ) of spleen DCs in the mice from ( h ) ( n = 5–7 mice per group). k Representative flow plots showing the percentages of neutrophils in the spleens of CLP-challenged WT mice subjected to different treatments. Quantification of the percentages ( l ) and absolute numbers ( m ) of splenic neutrophils in the mice in ( k ) ( n = 4–6 mice per group). n Representative immunofluorescence images showing the expression of NE and Ly6G in lung sections from CLP-challenged WT mice subjected to different treatments. Scale bars, 50 and 25 μm. o Quantification of NE-positive neutrophils in the lungs of ( n ) ( n = 6–7 mice per group). p Western blot analysis of citH3 in the lungs of CLP-challenged WT mice subjected to different treatments. q Quantification of protein levels in ( p ) ( n = 6–7 per group). r Quantitative analysis of neutrophil infiltration via measurement of MPO activity in lung tissue from CLP-challenged WT mice subjected to different treatments ( n = 6 mice per group). s Lung vascular permeability detected by EBD leakage in CLP-challenged WT mice subjected to different treatments ( n = 6 mice per group). Lung wet/dry weight ratio ( t ) ( n = 6 mice per group) and BALF protein levels ( u ) ( n = 6 mice per group) in CLP-challenged WT mice subjected to different treatments. v Representative histological images of lungs from CLP-challenged WT mice subjected to different treatments. Scale bars, 50 μm. w Quantification of lung injury scores on the basis of histological images from (v) ( n = 4–6 mice per group). Statistical significance was evaluated via one-way ANOVA followed by Tukey’s test for multiple comparisons ( f , g , i , j , l , m , o , q – u , w ) or two-way ANOVA followed by Tukey’s test for multiple comparisons ( d ) and the log-rank test ( e )

Article Snippet: After incubation with 5% bovine saline albumin in PBS for 30 min, the samples were incubated with primary antibodies against Ly6G/Ly6C (Invitrogen, Cat# 14-5931-82) and neutrophil elastase (ABclonal, Cat# A13015) for 12 h at 4 °C, followed by washing with PBS and incubation with Alexa Fluor 594- (Invitrogen, Cat# A-21207) or Alexa Fluor 488- (Invitrogen, Cat# A11008) for 2 h in the dark at room temperature.

Techniques: Activation Assay, Labeling, Clinical Proteomics, Immunofluorescence, Expressing, Western Blot, Activity Assay, Permeability