cxcl8  (Human Protein Atlas)

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Concentration-dependent change in the humoral inflammatory response following incubation with Escherichia coli ( E. coli ) in the ex vivo whole blood model. a Absolute plasma concentrations of IL-6, IL-8, and MMP9 determined by enzyme-linked immunosorbent assay. b Normalized values and EC 50 curve fit by BuC=0% and 50 000 CFU/ml E. coli= 100%, respectively, for IL-6, IL-8, and MMP9 as indicated by EC 50 (%) on the respective Y-axis. BuC indicates buffer control after 60 min incubation; numbers on the X-axis indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation; LPS indicates lipopolysaccharide (LPS) 100 ng/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, comparing all shown concentrations of E. coli bacteria and 100 ng/ml LPS with BuC. P -values are indicated above the respective data points. ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Concentration Assay, Incubation, Ex Vivo, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Bacteria

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Diagnostic performance for the detection of bacteremia, analyzing the neutrophil phenotype by determining the median fluorescence intensity (MFI) and the cellular response capacity (CRC) in comparison with traditional markers of humoral inflammation (IL-6, IL-8, MMP9). a Comparison of receiver operating characteristic (ROC) at 10,000 CFU/ml Escherichia coli ( E. coli ) with the respective 95% confidence interval (CI) and P -value, and half-maximal effective concentration (EC 50 ) as a function of the E. coli concentration. b Detailed comparison of the EC 50 as a function of the E. coli concentration. c Exemplary comparison of EC 50 curve fit after normalization as indicated by EC 50 (%) on the respective Y-axis to BuC=100% and 50 000 CFU/ml E. coli =0% for the humoral marker IL-6 (the IL-6 values were multiplied by −1 before EC 50 calculation to facilitate comparability with the CRC) and the change in neutrophil phenotype represented by CD11b CRC. BuC indicates buffer control after 60 min incubation; numbers on the X-axis of c indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, evaluating the EC 50 of IL-8, MMP9, the MFI, and CRC of CD10, CD11b, and CD62L in comparison to the EC 50 of IL-6. P -values are indicated above the respective data points. ⁎ P <0.05. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Diagnostic Assay, Fluorescence, Comparison, Concentration Assay, Marker, Control, Incubation, Bacteria

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Clinical specifications and parameters over all time points of the sepsis cohort. a Suspected infection cause of sepsis. b Distribution of the individual score points of the Sequential Organ Failure Assessment (SOFA) score. c Total SOFA score. d-h Traditional and humoral markers of inflammation: leukocytes and neutrophil-lymphocyte ratio ( d ), C-reactive protein (CRP) and procalcitonin (PCT) ( e ), interleukin-6 (IL-6) and interleukin-8 (IL-8) ( f ), serum amyloid A (SAA) and calprotectin ( g ), matrix metallopeptidase 9 (MMP9) and myeloperoxidase (MPO) ( h ). Values are shown as median and interquartile range. n =14. CNS. Central nervous system; HV. Healthy volunteers.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Infection

Journal: Cell Reports Medicine

Article Title: Predicting glioma survival and extracellular matrix remodeling through MRI radiogenomics

doi: 10.1016/j.xcrm.2026.102775

Figure Lengend Snippet: Functional analysis of radiogenomics landscape (A) After feature selection, the 11-feature radiomics signature exhibited the best diagnostic performance. The areas under the receiver operator characteristic curve (AUCs) curve were 0.886 in the training set, 0.845 in the test set, 0.828 in the validation set, and 0.904 in the 5-fold cross-validated (CV) training set. (B) The weighted coefficients of selected radiomics features. (C) The volcano plot and hierarchical clustering of differentially expressed genes (DEGs) between low- and high-Rad-score groups indicated that the landscape of genomics differed between low- and high-Rad-score groups. (D and E) The biological functional annotations for DEGs were performed by Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, as well as gene set enrichment analysis (GSEA). The top 10 radiogenomics-related biological processes were significantly correlated with the formation of ECM and activation of MMPs in GO-KEGG and GSEA. (F and G) Clustering and merging dendrogram of genes based on topological overlap performed by weighted gene co-expression network analysis (WGCNA) to identify the top 3 highest associated modules with Rad-score. Each row corresponds to a module eigengene with the corresponding correlation coefficient and p value from the left to the right side. (H and I) The most significant sub-network module and the top 10 genes with the highest maximum clique centrality score were identified by the “MCODE” and “CytoHubba” plug-in in Cytoscape. (J–M) (J and K) Hub genes had high connectivity. (L and M) Hub genes (MMP2, MMP9, CXCL8, TIMP1, IL-6, COL1A2, and CCL2) showed significantly up-regulated mRNA expression in the high-Rad-score group compared with the low-Rad-score group in both discovery and validation sets (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001).

Article Snippet: However, protein expression of CXCL8 and IL-6 was rarely detected in The Human Protein Atlas (THPA).

Techniques: Functional Assay, Selection, Diagnostic Assay, Biomarker Discovery, Activation Assay, Expressing

Journal: Cell Reports Medicine

Article Title: Predicting glioma survival and extracellular matrix remodeling through MRI radiogenomics

doi: 10.1016/j.xcrm.2026.102775

Figure Lengend Snippet: The protein expression patterns of radiogenomics-based hub genes (A) The protein expression patterns of 7 hub genes between normal brain tissues and glioma were determined by immunohistochemistry (IHC) staining from The Human Protein Atlas (THPA) database. Compared with normal brain tissues, the protein expression levels of hub genes increased in glioma as the grading of the tumor increased, except for CXCL8 and IL-6 without obvious detection. (B) IHC staining of acquired glioma specimens in proliferative core exhibited higher protein expression levels of MMP2, MMP9, TIMP1, COL1A2, and CCL2 in the high-Rad-score group. Compared with the hub gene labeling index (LI) in the low-Rad-score group, LIs of MMP2, TIMP1, and COL1A2 were significantly higher in the high-Rad-score group (∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001). (C) The expression levels and localization of MMP2, TIMP1, and COL1A2 were shown by the multiplex immunohistochemistry (mIHC) staining. The biological markers represented by different colors are labeled in the figure. The expression of the three genes increased in the high-Rad-score group, and MMP2 exhibited the most significant difference.

Article Snippet: However, protein expression of CXCL8 and IL-6 was rarely detected in The Human Protein Atlas (THPA).

Techniques: Expressing, Immunohistochemistry, Labeling, Multiplex Assay, Staining

Journal: Stem Cell Research & Therapy

Article Title: IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling

doi: 10.1186/s13287-026-05029-x

Figure Lengend Snippet: IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or ELISA. Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001

Article Snippet: All samples were diluted 1:1 and the analytes were measured using custom made cartridges that included CCL2, CXCL5, and CXCL8 (Bio-techne) or measured by Quantikine ELISA (cat# D8000C, R&D Systems) with 1:1 dilution.

Techniques: Expressing, Control, Enzyme-linked Immunosorbent Assay, Derivative Assay

Journal: bioRxiv

Article Title: PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling

doi: 10.64898/2026.04.21.719931

Figure Lengend Snippet: ( a ) Cell viability was assessed with the MTT assay and data shown are means ± SD (n = 3). ( b ) TNFα, IL-6 and IL-8 expression in response to B[a]P exposure. ( c ) Representative Western blot images showing protein expression. All data were obtained from three independent experiments. Statistical p values were determined by a one-way ANOVA, followed by a Tukey post-hoc test comparing the B[a]P treatments to the DMSO control; * p < 0.05; ¥, p < 0.01; NS, no significance.

Article Snippet: Benzo[a]pyrene, PM 2.5 (ERMCZ110), CFTR inh -172, IBMX, amiloride, Forskolin, MG-132, L-glutathione, and Millipore Immobilon Western (Sigma-Aldrich); BI 749327, LY 294002, and LY 303511 (Cayman Chemical); MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide; EZ-LinkTM Sulfo-NHS-SS-Biotin, CellROX green reagent, Dynabeads Protein G, Pierce Streptavidin magnetic beads, HaltTM protease and Phosphatase Inhibitor Cocktail (Thermo Fisher) ; Fluo-4 AM and Probenecid (Invitrogen); Human IL-8/CXCL8 DuoSet® ELISA kit, Human IL-6 ELISA DuoSet® kit, and Human TNF-alpha DuoSet® ELISA (R&D Systems); Ferret IL-6 ELISA kit (Genorise, PA, USA); Pneumacult-ALI media kit and Pneumacult-EX Plus Basal media kit (Stemcell); and Gibco MEM (Thermo Fisher).

Techniques: MTT Assay, Expressing, Western Blot, Control

Journal: bioRxiv

Article Title: PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling

doi: 10.64898/2026.04.21.719931

Figure Lengend Snippet: Cells were treated with various concentrations of PM2.5 for 24 hr. ( a ) Cell viability was assessed with MTT assay. ( b ) IL-6 and IL-8 from the basolateral sides. ( c ) Representative Western blot images showing CFTR, β2AR, phospho-AKT (Ser473), AKT, phospho-NF-κB p65 (Ser536), NF-κB p65, and TRPC6 expression. All data are presented as the mean ± SD (n = 4). Statistical p values were determined with a one-way ANOVA, followed by the Tukey post-hoc test comparing the B[a]P or PM 2.5 treatments to the DMSO control; *, p < 0.05; ¥, p < 0.01; NS, no significance.

Article Snippet: Benzo[a]pyrene, PM 2.5 (ERMCZ110), CFTR inh -172, IBMX, amiloride, Forskolin, MG-132, L-glutathione, and Millipore Immobilon Western (Sigma-Aldrich); BI 749327, LY 294002, and LY 303511 (Cayman Chemical); MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide; EZ-LinkTM Sulfo-NHS-SS-Biotin, CellROX green reagent, Dynabeads Protein G, Pierce Streptavidin magnetic beads, HaltTM protease and Phosphatase Inhibitor Cocktail (Thermo Fisher) ; Fluo-4 AM and Probenecid (Invitrogen); Human IL-8/CXCL8 DuoSet® ELISA kit, Human IL-6 ELISA DuoSet® kit, and Human TNF-alpha DuoSet® ELISA (R&D Systems); Ferret IL-6 ELISA kit (Genorise, PA, USA); Pneumacult-ALI media kit and Pneumacult-EX Plus Basal media kit (Stemcell); and Gibco MEM (Thermo Fisher).

Techniques: MTT Assay, Western Blot, Expressing, Control

Journal: bioRxiv

Article Title: PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling

doi: 10.64898/2026.04.21.719931

Figure Lengend Snippet: ( a ) IL-6 and IL-8 from the basolateral sides of the ALI were determined using the DuoSet® ELISA kits. Data are presented as the mean ± SD (n = 4). Statistical p -values were determined with a one-way ANOVA, followed by the Tukey post-hoc test comparing the all treatments to the DMSO control; ¥, p < 0.05; *, p < 0.01. ( b ) Representative Western blot images showing CFTR, phospho-AKT (Ser473), AKT, phospho-NF-κB p65 (Ser536), and NF-κB p65 expression in treated polarized 16HBE14o-cells in ( a ). All data were obtained from three independent experiments.

Article Snippet: Benzo[a]pyrene, PM 2.5 (ERMCZ110), CFTR inh -172, IBMX, amiloride, Forskolin, MG-132, L-glutathione, and Millipore Immobilon Western (Sigma-Aldrich); BI 749327, LY 294002, and LY 303511 (Cayman Chemical); MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide; EZ-LinkTM Sulfo-NHS-SS-Biotin, CellROX green reagent, Dynabeads Protein G, Pierce Streptavidin magnetic beads, HaltTM protease and Phosphatase Inhibitor Cocktail (Thermo Fisher) ; Fluo-4 AM and Probenecid (Invitrogen); Human IL-8/CXCL8 DuoSet® ELISA kit, Human IL-6 ELISA DuoSet® kit, and Human TNF-alpha DuoSet® ELISA (R&D Systems); Ferret IL-6 ELISA kit (Genorise, PA, USA); Pneumacult-ALI media kit and Pneumacult-EX Plus Basal media kit (Stemcell); and Gibco MEM (Thermo Fisher).

Techniques: Enzyme-linked Immunosorbent Assay, Control, Western Blot, Expressing

Journal: bioRxiv

Article Title: PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling

doi: 10.64898/2026.04.21.719931

Figure Lengend Snippet: ALI cells were treated with DMSO, 100 ng/mL PM 2.5, 10 µM LY 294002 ± PM 2.5, or 10 µM LY 303511 ± PM 2.5 for 24 hrs. ( a ) IL-6 and IL-8 from the basolateral sides were determined using the DuoSet® ELISA kits. Data are presented as the mean ± SD (n=3). Statistical p values were determined with a one-way ANOVA, followed by the Tukey post-hoc test comparing all treatments to the DMSO control, or PM 2.5 to PM 2.5 ± LY 294002 or LY 303511; *, p < 0.01. ( b ) Representative Western blot images showing CFTR and β-actin expression. β-actin was used to ensure equal loading of protein. All data were obtained from three independent experiments, and each experiment was analyzed in duplication.

Article Snippet: Benzo[a]pyrene, PM 2.5 (ERMCZ110), CFTR inh -172, IBMX, amiloride, Forskolin, MG-132, L-glutathione, and Millipore Immobilon Western (Sigma-Aldrich); BI 749327, LY 294002, and LY 303511 (Cayman Chemical); MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide; EZ-LinkTM Sulfo-NHS-SS-Biotin, CellROX green reagent, Dynabeads Protein G, Pierce Streptavidin magnetic beads, HaltTM protease and Phosphatase Inhibitor Cocktail (Thermo Fisher) ; Fluo-4 AM and Probenecid (Invitrogen); Human IL-8/CXCL8 DuoSet® ELISA kit, Human IL-6 ELISA DuoSet® kit, and Human TNF-alpha DuoSet® ELISA (R&D Systems); Ferret IL-6 ELISA kit (Genorise, PA, USA); Pneumacult-ALI media kit and Pneumacult-EX Plus Basal media kit (Stemcell); and Gibco MEM (Thermo Fisher).

Techniques: Enzyme-linked Immunosorbent Assay, Control, Western Blot, Expressing

Journal: bioRxiv

Article Title: PM2.5 toxin benzo[a]pyrene induces life-limiting inflammation and oxidative stress in the airway by up-regulation of TRPC6 and inactivation of β2AR/CFTR signaling

doi: 10.64898/2026.04.21.719931

Figure Lengend Snippet: ( a ) The lung parenchyma from two ferrets were sliced into several sections as shown. Arrows indicate the tracheobronchial tubes. All tissue sections were incubating with DMSO (control), 10 µM B[a]P, or 100 ng/mL PM 2.5 in Pneumacult-EX Plus Basal media for 24 hrs. ( b ) IL 6 secretion was determined using the ferret ELISA kit. Data represent the mean of 6 independent sections. Statistical p values were determined with a one-way ANOVA, followed by the Tukey post-hoc test comparing the B[a]P or PM 2.5 treatments to the DMSO control; ¥, p < 0.05 (n = 6). ( c ) Representative western blotting images show reduction of CFTR, and β2AR and elevation of TRPC6 expression in explants under these treatments.

Article Snippet: Benzo[a]pyrene, PM 2.5 (ERMCZ110), CFTR inh -172, IBMX, amiloride, Forskolin, MG-132, L-glutathione, and Millipore Immobilon Western (Sigma-Aldrich); BI 749327, LY 294002, and LY 303511 (Cayman Chemical); MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide; EZ-LinkTM Sulfo-NHS-SS-Biotin, CellROX green reagent, Dynabeads Protein G, Pierce Streptavidin magnetic beads, HaltTM protease and Phosphatase Inhibitor Cocktail (Thermo Fisher) ; Fluo-4 AM and Probenecid (Invitrogen); Human IL-8/CXCL8 DuoSet® ELISA kit, Human IL-6 ELISA DuoSet® kit, and Human TNF-alpha DuoSet® ELISA (R&D Systems); Ferret IL-6 ELISA kit (Genorise, PA, USA); Pneumacult-ALI media kit and Pneumacult-EX Plus Basal media kit (Stemcell); and Gibco MEM (Thermo Fisher).

Techniques: Control, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing

Journal: Stem Cell Research & Therapy

Article Title: IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling

doi: 10.1186/s13287-026-05029-x

Figure Lengend Snippet: IL-1β stimulation changes the transcriptomic profile of BM-hMSCs. Schematic of experimental design A . BM-hMSCs were exposed to IL-1 β (3 replicates, 1 donor) or left unstimulated (3 replicates, 1 donor) for one hour, followed by bulk RNA sequencing. PCA plot was used to show the variance between the unstimulated control (green) and IL-1 β exposed (purple) samples B . Heatmap displaying the Z-score of the top 100 varying genes across all samples. Red color indicates higher expression of the genes and blue color indicates decreased expression C . Volcano plot of differentially expressed genes, showing their log2 fold change (X-axis) and -log10 adjusted p-values (Y-axis) D . IL-1 β Interleukin-1β, BM-hMSCs, Bone marrow derived human mesenchymal cells, PCA Principal component analysis, FC Fold change, NS not significant. Figure 1A was created using Biorender.com

Article Snippet: Following synchronization, medium was removed, and cells were stimulated with IL-1β (20 ng/ml in DPBS with 0.1% Bovine Serum Albumin, cat# 208-IL-010, R&D Systems) for 1 h (RNA-sequencing) or 24 h. Unstimulated control BM-hMSCs were exposed to serum free DMEM only.

Techniques: RNA Sequencing, Control, Expressing, Derivative Assay

Journal: Stem Cell Research & Therapy

Article Title: IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling

doi: 10.1186/s13287-026-05029-x

Figure Lengend Snippet: IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or ELISA. Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001

Article Snippet: Following synchronization, medium was removed, and cells were stimulated with IL-1β (20 ng/ml in DPBS with 0.1% Bovine Serum Albumin, cat# 208-IL-010, R&D Systems) for 1 h (RNA-sequencing) or 24 h. Unstimulated control BM-hMSCs were exposed to serum free DMEM only.

Techniques: Expressing, Control, Enzyme-linked Immunosorbent Assay, Derivative Assay

Journal: Stem Cell Research & Therapy

Article Title: IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling

doi: 10.1186/s13287-026-05029-x

Figure Lengend Snippet: IL-1β stimulated BM-hMSCs increased neutrophil recruitment partly via the NF-kB signaling pathway. Schematic of experimental design of the neutrophil migration assay. Illustration was created with BioRender.com A . Number of neutrophils that migrated through the transwell membrane from the top well to the bottom towards control conditioned medium, conditioned medium from IL-1β stimulated BM-hMSCs, and conditioned medium from IL-1β with the NF-kB inhibitor stimulated BM-hMSCs. The experiment was performed using neutrophils from four different donors (each donor represent one data point) and the experiments were performed on three different days. B . Protein expression of CXCL1 was measured in conditioned medium from unstimulated BM-hMSCs (4 replicates, 1 donor, green), IL-1β stimulated BM-hMSCs (4 replicates, 1 donor, purple), and ILβ stimulated BM-hMSCs with 10 μM BAY 11–7082 (4 replicates, 1 donor, grey) C . Phospho-p65 levels were quantified and normalized to total p65. Data are expressed relative to control, which was set to 1 D . IL-1β Interleukin-1β BM-hMSCs Bone marrow-derived human mesenchymal cells, Ctrl control, CXCL1 chemokine (C-X-C motif) ligand 1, ns not significant; * p < 0,05; ****, p < 0,0001

Article Snippet: Following synchronization, medium was removed, and cells were stimulated with IL-1β (20 ng/ml in DPBS with 0.1% Bovine Serum Albumin, cat# 208-IL-010, R&D Systems) for 1 h (RNA-sequencing) or 24 h. Unstimulated control BM-hMSCs were exposed to serum free DMEM only.

Techniques: Migration, Membrane, Control, Expressing, Derivative Assay