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R&D Systems s100a8 a9 heterodimer

Klebsiella pneumoniae infection directly <t>induces</t> <t>S100A8/A9</t> expression and secretion in HBE cells. Primary HBE cells were infected with WT K. pneumoniae or an isogenic acapsular mutant (Δ cps ). (A,B) Expression of S100A8 and S100A9 was determined by qRT-PCR at 8 h post-infection with various MOIs of K. pneumoniae , or 100 MOI K. pneumoniae for 4–12 h (C,D) . Data are normalized to the housekeeping gene GAPDH and expressed as fold change relative to uninfected control cells. (E) Secretion of S100A8/A9 heterodimer induced by WT K. pneumoniae and the isogenic Δ cps mutant at indicated MOIs after 24 h. All data are presented as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01 vs. uninfected cells (A–D) . Statistical differences between the WT and Δ cps groups were determined by Two-way ANOVA followed by Tukey’s post-hoc test. * p < 0.05 compared between strains at the same MOI (E) .

S100a8 A9 Heterodimer, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/s100a8+a9/Human+S100A8%2FS100A9+Heterodimer+Quantikine+ELISA+Kit/pmc12992257-59-4-16
Average 95 stars, based on 41 article reviews

s100a8 a9 heterodimer - by Bioz Stars, 2026-09

95/100 stars

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1) Product Images from "Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation"

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

Journal: Frontiers in Microbiology

doi: 10.3389/fmicb.2026.1768140

Klebsiella pneumoniae infection directly induces S100A8/A9 expression and secretion in HBE cells. Primary HBE cells were infected with WT K. pneumoniae or an isogenic acapsular mutant (Δ cps ). (A,B) Expression of S100A8 and S100A9 was determined by qRT-PCR at 8 h post-infection with various MOIs of K. pneumoniae , or 100 MOI K. pneumoniae for 4–12 h (C,D) . Data are normalized to the housekeeping gene GAPDH and expressed as fold change relative to uninfected control cells. (E) Secretion of S100A8/A9 heterodimer induced by WT K. pneumoniae and the isogenic Δ cps mutant at indicated MOIs after 24 h. All data are presented as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01 vs. uninfected cells (A–D) . Statistical differences between the WT and Δ cps groups were determined by Two-way ANOVA followed by Tukey’s post-hoc test. * p < 0.05 compared between strains at the same MOI (E) .

Figure Legend Snippet: Klebsiella pneumoniae infection directly induces S100A8/A9 expression and secretion in HBE cells. Primary HBE cells were infected with WT K. pneumoniae or an isogenic acapsular mutant (Δ cps ). (A,B) Expression of S100A8 and S100A9 was determined by qRT-PCR at 8 h post-infection with various MOIs of K. pneumoniae , or 100 MOI K. pneumoniae for 4–12 h (C,D) . Data are normalized to the housekeeping gene GAPDH and expressed as fold change relative to uninfected control cells. (E) Secretion of S100A8/A9 heterodimer induced by WT K. pneumoniae and the isogenic Δ cps mutant at indicated MOIs after 24 h. All data are presented as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01 vs. uninfected cells (A–D) . Statistical differences between the WT and Δ cps groups were determined by Two-way ANOVA followed by Tukey’s post-hoc test. * p < 0.05 compared between strains at the same MOI (E) .

Techniques Used: Infection, Expressing, Mutagenesis, Quantitative RT-PCR, Control

Extracellular S100A8/A9 functions as a potent pro-inflammatory stimulus for primary HBE cells. (A) Primary HBE cells were infected with WT K. pneumoniae (MOI 100) for the indicated time points. Relative mRNA expression of TLR4 was determined by qRT-PCR, with data calibrated to GAPDH and shown as fold induction over the baseline (0 h). (B) Representative western blot showing total TLR4 protein levels. β -Actin served as the housekeeping protein. (C) Quantification of TLR4 protein expression from three independent replicates, with values standardized to β-Actin. (D,E) HBE cells were treated for 24 h with the specified doses of endotoxin-free recombinant human S100A8/A9 (rS100A8/A9). The release of (D) IL-8 and (E) IL-6 was detected by ELISA. Data are presented as mean ± SEM of three independent experiments. * p < 0.05 versus the untreated control (A,C,D,E) .

Figure Legend Snippet: Extracellular S100A8/A9 functions as a potent pro-inflammatory stimulus for primary HBE cells. (A) Primary HBE cells were infected with WT K. pneumoniae (MOI 100) for the indicated time points. Relative mRNA expression of TLR4 was determined by qRT-PCR, with data calibrated to GAPDH and shown as fold induction over the baseline (0 h). (B) Representative western blot showing total TLR4 protein levels. β -Actin served as the housekeeping protein. (C) Quantification of TLR4 protein expression from three independent replicates, with values standardized to β-Actin. (D,E) HBE cells were treated for 24 h with the specified doses of endotoxin-free recombinant human S100A8/A9 (rS100A8/A9). The release of (D) IL-8 and (E) IL-6 was detected by ELISA. Data are presented as mean ± SEM of three independent experiments. * p < 0.05 versus the untreated control (A,C,D,E) .

Techniques Used: Infection, Expressing, Quantitative RT-PCR, Western Blot, Recombinant, Enzyme-linked Immunosorbent Assay, Control

Epithelial-derived S100A8/A9 is functionally required for the full inflammatory response to K. pneumoniae infection. Primary HBE cells were transfected with control siRNA (siCtrl) or S100A9 siRNA (siA9). (A) Knockdown efficiency was confirmed 48 h post-transfection by qRT-PCR analysis of S100A9 mRNA levels following a 12-h infection with WT K. pneumoniae (MOI 100), negative values represent fold reduction calculated as the negative inverse of 2 −ΔΔCt following the Schmittgen and Livak protocol. (B) Functional knockdown was confirmed by measuring S100A8/A9 protein secretion by ELISA in supernatants from infected cells at 24 h. (C,D) Control and S100A9 -deficient cells were infected with WT K. pneumoniae (MOI 100) for 24 h, and the secretion of cytokines were quantified by ELISA. Data are presented as mean ± SEM of three independent experiments. * p < 0.05 vs. Kp + siCtrl (A,B) or uninfected cells (C,D) , # p < 0.05 vs. Kp + siCtrl (C,D) .

Figure Legend Snippet: Epithelial-derived S100A8/A9 is functionally required for the full inflammatory response to K. pneumoniae infection. Primary HBE cells were transfected with control siRNA (siCtrl) or S100A9 siRNA (siA9). (A) Knockdown efficiency was confirmed 48 h post-transfection by qRT-PCR analysis of S100A9 mRNA levels following a 12-h infection with WT K. pneumoniae (MOI 100), negative values represent fold reduction calculated as the negative inverse of 2 −ΔΔCt following the Schmittgen and Livak protocol. (B) Functional knockdown was confirmed by measuring S100A8/A9 protein secretion by ELISA in supernatants from infected cells at 24 h. (C,D) Control and S100A9 -deficient cells were infected with WT K. pneumoniae (MOI 100) for 24 h, and the secretion of cytokines were quantified by ELISA. Data are presented as mean ± SEM of three independent experiments. * p < 0.05 vs. Kp + siCtrl (A,B) or uninfected cells (C,D) , # p < 0.05 vs. Kp + siCtrl (C,D) .

Techniques Used: Derivative Assay, Infection, Transfection, Control, Knockdown, Quantitative RT-PCR, Functional Assay, Enzyme-linked Immunosorbent Assay

TLR4 is the essential receptor mediating S100A8/A9-induced inflammation in HBE cells during K. pneumoniae infection. (A,B) HBE cells were pre-incubated with neutralizing antibodies against TLR4 (10 μg/mL), RAGE (100 μg/mL), or an isotype control (Iso Ctrl) for 1 h, followed by stimulation with recombinant human S100A8/A9 (20 μg/mL) for 24 h. Levels of (A) IL-8 and (B) IL-6 in supernatants were determined by ELISA. (C,D) HBE cells were pre-treated with the indicated antibodies for 1 h and subsequently infected with WT K. pneumoniae (MOI 100) for 24 h. Secretion of (C) IL-8 and (D) IL-6 was quantified by ELISA. All results are expressed as mean ± SEM of three independent experiments. * p < 0.05 compared with the indicated groups.

Figure Legend Snippet: TLR4 is the essential receptor mediating S100A8/A9-induced inflammation in HBE cells during K. pneumoniae infection. (A,B) HBE cells were pre-incubated with neutralizing antibodies against TLR4 (10 μg/mL), RAGE (100 μg/mL), or an isotype control (Iso Ctrl) for 1 h, followed by stimulation with recombinant human S100A8/A9 (20 μg/mL) for 24 h. Levels of (A) IL-8 and (B) IL-6 in supernatants were determined by ELISA. (C,D) HBE cells were pre-treated with the indicated antibodies for 1 h and subsequently infected with WT K. pneumoniae (MOI 100) for 24 h. Secretion of (C) IL-8 and (D) IL-6 was quantified by ELISA. All results are expressed as mean ± SEM of three independent experiments. * p < 0.05 compared with the indicated groups.

Techniques Used: Infection, Incubation, Control, Recombinant, Enzyme-linked Immunosorbent Assay

The S100A8/A9 autocrine loop drives NF-κB activation and subsequent cytokine release in HBE cells. (A) Representative immunoblots showing degradation of IκBα in primary HBE cells stimulated with rS100A8/A9 (20 μg/mL) for 60 min. β-Actin served as a loading control. (B) Densitometric quantification of IκBα protein levels from (A) . (C) Representative immunofluorescence images showing subcellular localization of the p65 subunit (green) at 60 min post-stimulation with rS100A8/A9. Nuclei were counterstained with DAPI (blue). (D) HBE cells were transfected with control siRNA (siCtrl) or siRNA targeting S100A9 (siS100A9) and subsequently infected with wild-type K. pneumoniae (MOI 100). Representative immunoblots of IκBα levels are shown at 60 min post-infection. (E) Densitometric quantification of IκBα degradation from (D) . (F) Representative immunofluorescence images showing p65 localization (green) in siCtrl- or siS100A9-transfected HBE cells at 60 min post- K. pneumoniae infection. Nuclei were stained with DAPI (blue). (G) Secretion of IL-8 and IL-6 by HBE cells. Cells were pre-treated with or without the NF-κB inhibitor BAY 11–7,082 (10 μM) for 60 min, followed by stimulation with rS100A8/A9 (20 μg/mL) for 24 h. Cytokine levels in supernatants were measured by ELISA. All graphs display mean ± SEM, * p < 0.05 compared with the untreated control (B,E,G) ; # p < 0.05 compared with siCtrl + Kp or the S100A8/A9-stimulated group without inhibitor (E,G) .

Figure Legend Snippet: The S100A8/A9 autocrine loop drives NF-κB activation and subsequent cytokine release in HBE cells. (A) Representative immunoblots showing degradation of IκBα in primary HBE cells stimulated with rS100A8/A9 (20 μg/mL) for 60 min. β-Actin served as a loading control. (B) Densitometric quantification of IκBα protein levels from (A) . (C) Representative immunofluorescence images showing subcellular localization of the p65 subunit (green) at 60 min post-stimulation with rS100A8/A9. Nuclei were counterstained with DAPI (blue). (D) HBE cells were transfected with control siRNA (siCtrl) or siRNA targeting S100A9 (siS100A9) and subsequently infected with wild-type K. pneumoniae (MOI 100). Representative immunoblots of IκBα levels are shown at 60 min post-infection. (E) Densitometric quantification of IκBα degradation from (D) . (F) Representative immunofluorescence images showing p65 localization (green) in siCtrl- or siS100A9-transfected HBE cells at 60 min post- K. pneumoniae infection. Nuclei were stained with DAPI (blue). (G) Secretion of IL-8 and IL-6 by HBE cells. Cells were pre-treated with or without the NF-κB inhibitor BAY 11–7,082 (10 μM) for 60 min, followed by stimulation with rS100A8/A9 (20 μg/mL) for 24 h. Cytokine levels in supernatants were measured by ELISA. All graphs display mean ± SEM, * p < 0.05 compared with the untreated control (B,E,G) ; # p < 0.05 compared with siCtrl + Kp or the S100A8/A9-stimulated group without inhibitor (E,G) .

Techniques Used: Activation Assay, Western Blot, Control, Immunofluorescence, Transfection, Infection, Staining, Enzyme-linked Immunosorbent Assay

The epithelial S100A8/A9 autocrine loop is a critical driver of neutrophil chemotaxis in response to K. pneumoniae infection. Neutrophil chemotaxis was assessed using a Transwell assay. (A) Comparison of the chemotactic activity of supernatants from uninfected HBE cells (conditioned medium, CM), HBE cells infected with WT K. pneumoniae (MOI 100), and fMLP (positive control) on primary human neutrophils. (B) Comparison of the chemotactic activity of supernatants from infected control (siCtrl) HBE cells versus infected S100A9-deficient (siS100A9) HBE cells. Flow cytometry was used to determine the absolute number of migrated neutrophils. Data are shown as mean ± SEM from three separate experiments. * p < 0.05 vs. uninfected CM, # p < 0.05 vs. Kp + siCtrl.

Figure Legend Snippet: The epithelial S100A8/A9 autocrine loop is a critical driver of neutrophil chemotaxis in response to K. pneumoniae infection. Neutrophil chemotaxis was assessed using a Transwell assay. (A) Comparison of the chemotactic activity of supernatants from uninfected HBE cells (conditioned medium, CM), HBE cells infected with WT K. pneumoniae (MOI 100), and fMLP (positive control) on primary human neutrophils. (B) Comparison of the chemotactic activity of supernatants from infected control (siCtrl) HBE cells versus infected S100A9-deficient (siS100A9) HBE cells. Flow cytometry was used to determine the absolute number of migrated neutrophils. Data are shown as mean ± SEM from three separate experiments. * p < 0.05 vs. uninfected CM, # p < 0.05 vs. Kp + siCtrl.

Techniques Used: Chemotaxis Assay, Infection, Transwell Assay, Comparison, Activity Assay, Positive Control, Control, Flow Cytometry

Proposed model of the S100A8/A9-mediated autocrine amplification loop in human airway epithelial cells during K. pneumoniae infection. Initial recognition of encapsulated K. pneumoniae by the airway epithelium triggers a primary transcriptional response, leading to the synthesis and secretion of the alarmin S100A8/A9 and a simultaneous upregulation of its cognate receptor, TLR4. This dual mechanism creates a primed state within the epithelium. The endogenously produced S100A8/A9 then acts back on the enriched TLR4 receptors in an autocrine or paracrine manner, activating the canonical NF-κB signaling pathway (characterized by IκB degradation and p65 nuclear translocation). This positive feedback loop significantly magnifies the production of pro-inflammatory cytokines such as IL-6 and IL-8, ultimately orchestrating massive neutrophil recruitment and driving the hyper-inflammation observed in severe pneumonia. Created in BioRender [You (2026) https://BioRender.com/qo9szis ].

Figure Legend Snippet: Proposed model of the S100A8/A9-mediated autocrine amplification loop in human airway epithelial cells during K. pneumoniae infection. Initial recognition of encapsulated K. pneumoniae by the airway epithelium triggers a primary transcriptional response, leading to the synthesis and secretion of the alarmin S100A8/A9 and a simultaneous upregulation of its cognate receptor, TLR4. This dual mechanism creates a primed state within the epithelium. The endogenously produced S100A8/A9 then acts back on the enriched TLR4 receptors in an autocrine or paracrine manner, activating the canonical NF-κB signaling pathway (characterized by IκB degradation and p65 nuclear translocation). This positive feedback loop significantly magnifies the production of pro-inflammatory cytokines such as IL-6 and IL-8, ultimately orchestrating massive neutrophil recruitment and driving the hyper-inflammation observed in severe pneumonia. Created in BioRender [You (2026) https://BioRender.com/qo9szis ].

Techniques Used: Amplification, Infection, Produced, Translocation Assay

Derivative Assay:

Article Title: Sterile triggers drive joint inflammation in TNF- and IL-1β-dependent mouse arthritis models.
Article Snippet: .. After 3–5 passages, cells were seeded and stimulated for 48 h with either HMGB1 (Abcam; ab255799, 100 ng/ml), uric acid 2023 The Authors EMBO Molecular Medicine 15: e17691 | 2023 13 of 17 D ow nloaded from https://w w w .em bopress.org on January 18, 2024 from IP 175.176.52.48. (Sigma Aldrich, U2625-25G, 200 lM), S100A8/A9 (R&D Systems; 8916-S8, 100 ng/ml), a combination of HMGB1, uric acid, and S100A8/A9 or a crude mix of intracellular DAMPs derived from freeze-thawed cells (crude cell lysate, 2,500,000 cells/ml). ..

Article Title: Sterile triggers drive joint inflammation in TNF‐ and IL ‐1β‐dependent mouse arthritis models
Article Snippet: .. After 3–5 passages, cells were seeded and stimulated for 48 h with either HMGB1 (Abcam; ab255799, 100 ng/ml), uric acid (Sigma Aldrich, U2625‐25G, 200 μM), S100A8/A9 (R&D Systems; 8916‐S8, 100 ng/ml), a combination of HMGB1, uric acid, and S100A8/A9 or a crude mix of intracellular DAMPs derived from freeze‐thawed cells (crude cell lysate, 2,500,000 cells/ml). ..

Enzyme-linked Immunosorbent Assay:

Article Title: INTERCELLULAR HIF1α REPROGAMS MAMMARY PROGENITORS AND MYELOID IMMUNE EVASION TO DRIVE HIGH-RISK BREAST LESIONS
Article Snippet: .. S100A8/A9 was measured by Mouse S100A8/S100A9 Heterodimer DuoSet ELISA (R&D System, Minneapolis, MN, USA) according to manufacturer instruction. ..

Article Title: Clonally expanded IgG antibody-secreting cells preferentially target influenza nucleoprotein following homologous and heterologous infections
Article Snippet: .. High-binding ELISA plates were coated with Mucin 5AC (abx068104, Abbexa), S100A8/A9 (8916-S8-050, R&D Systems), LPS (tlrl-pglps, InvivoGen), Flagellin (tlrl-stfla, InvivoGen), Mog1-125 (AS-55150-100, Anaspec), hTNFR2 (310-12, Peprotech), Ovalbumin (A5503, Sigma), Calf Thymus DNA (15633019, Thermo) at 10 μg ml−1 in PBS, Fecal bacteria and tissue lysates (lung, brain, colon and small intestine). ..

Article Title: Clonally expanded IgG, but not IgA, antibody-secreting cells preferentially target influenza nucleoprotein following homologous and heterologous infections.
Article Snippet: Infection with influenza virus remains a significant global health concern due to its ability to acquire mutations at key antigenic sites to escape antibody recognition.. While germinal center (GC) and memory B cells have been well studied following influenza infection, the clonal dynamics of antibody secreting cells (ASCs), particularly those within the bone marrow (BM) niche that are responsible for serum immune protection, remain poorly understood.. Here, we combine single-cell RNA (scRNA) and B cell receptor (BCR) sequencing to characterize individual ASCs following various Influenza exposure histories.

Article Title: Development of Luminescent Biosensors for Calprotectin
Article Snippet: .. For the serums from 4 TB patients and 4 healthy controls, circulating levels of S100A8/A9 were measured in serum samples by ELISA using the DuoSet ELISA Development Kit for human S100A8/S100A9 heterodimer (catalog DY8226, R&D Systems Inc.), according to the manufacturer’s instructions. ..

Bacteria:

Image Search Results

Baseline Characteristics of Healthy Controls (HCs), Patients Without Sepsis-Related Liver Injury (SRLI), or Patients Without Sepsis-Related Liver Injury (Non-SRLI)

Journal: Journal of Inflammation Research

Article Title: S100A8/A9 Inhibition Reduces Neutrophil Extracellular Trap Formation and Mitigates Sepsis-Related Liver Injury

doi: 10.2147/JIR.S609689

Figure Lengend Snippet: Baseline Characteristics of Healthy Controls (HCs), Patients Without Sepsis-Related Liver Injury (SRLI), or Patients Without Sepsis-Related Liver Injury (Non-SRLI)

Article Snippet: To investigate the effect of S100A8/A9 on SRLI, wild-type mice were intraperitoneally injected with the S100A8/A9 inhibitor paquinimod (MedChemExpress, Monmouth Junction, NJ, USA) at a dose of 10 mg/kg 24 h before CLP or sham surgery.

Techniques:

Receiver Operating Characteristic (ROC) Curve Analysis Results of S100A8/A9 on Patients Without Sepsis-Related Liver Injury (SRLI)

Journal: Journal of Inflammation Research

Article Title: S100A8/A9 Inhibition Reduces Neutrophil Extracellular Trap Formation and Mitigates Sepsis-Related Liver Injury

doi: 10.2147/JIR.S609689

Figure Lengend Snippet: Receiver Operating Characteristic (ROC) Curve Analysis Results of S100A8/A9 on Patients Without Sepsis-Related Liver Injury (SRLI)

Techniques:

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Figure Lengend Snippet: Klebsiella pneumoniae infection directly induces S100A8/A9 expression and secretion in HBE cells. Primary HBE cells were infected with WT K. pneumoniae or an isogenic acapsular mutant (Δ cps ). (A,B) Expression of S100A8 and S100A9 was determined by qRT-PCR at 8 h post-infection with various MOIs of K. pneumoniae , or 100 MOI K. pneumoniae for 4–12 h (C,D) . Data are normalized to the housekeeping gene GAPDH and expressed as fold change relative to uninfected control cells. (E) Secretion of S100A8/A9 heterodimer induced by WT K. pneumoniae and the isogenic Δ cps mutant at indicated MOIs after 24 h. All data are presented as mean ± SEM of three independent experiments. * p < 0.05, ** p < 0.01 vs. uninfected cells (A–D) . Statistical differences between the WT and Δ cps groups were determined by Two-way ANOVA followed by Tukey’s post-hoc test. * p < 0.05 compared between strains at the same MOI (E) .

Article Snippet: The concentrations of secreted S100A8/A9 heterodimer, IL-8, and IL-6 were quantified by commercial Quantikine ELISA kits (R&D Systems, Cat# DS8900 for S100A8/A9, D8000C for IL-8, and D6050B for IL-6).

Techniques: Infection, Expressing, Mutagenesis, Quantitative RT-PCR, Control

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Figure Lengend Snippet: Extracellular S100A8/A9 functions as a potent pro-inflammatory stimulus for primary HBE cells. (A) Primary HBE cells were infected with WT K. pneumoniae (MOI 100) for the indicated time points. Relative mRNA expression of TLR4 was determined by qRT-PCR, with data calibrated to GAPDH and shown as fold induction over the baseline (0 h). (B) Representative western blot showing total TLR4 protein levels. β -Actin served as the housekeeping protein. (C) Quantification of TLR4 protein expression from three independent replicates, with values standardized to β-Actin. (D,E) HBE cells were treated for 24 h with the specified doses of endotoxin-free recombinant human S100A8/A9 (rS100A8/A9). The release of (D) IL-8 and (E) IL-6 was detected by ELISA. Data are presented as mean ± SEM of three independent experiments. * p < 0.05 versus the untreated control (A,C,D,E) .

Techniques: Infection, Expressing, Quantitative RT-PCR, Western Blot, Recombinant, Enzyme-linked Immunosorbent Assay, Control

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Figure Lengend Snippet: Epithelial-derived S100A8/A9 is functionally required for the full inflammatory response to K. pneumoniae infection. Primary HBE cells were transfected with control siRNA (siCtrl) or S100A9 siRNA (siA9). (A) Knockdown efficiency was confirmed 48 h post-transfection by qRT-PCR analysis of S100A9 mRNA levels following a 12-h infection with WT K. pneumoniae (MOI 100), negative values represent fold reduction calculated as the negative inverse of 2 −ΔΔCt following the Schmittgen and Livak protocol. (B) Functional knockdown was confirmed by measuring S100A8/A9 protein secretion by ELISA in supernatants from infected cells at 24 h. (C,D) Control and S100A9 -deficient cells were infected with WT K. pneumoniae (MOI 100) for 24 h, and the secretion of cytokines were quantified by ELISA. Data are presented as mean ± SEM of three independent experiments. * p < 0.05 vs. Kp + siCtrl (A,B) or uninfected cells (C,D) , # p < 0.05 vs. Kp + siCtrl (C,D) .

Techniques: Derivative Assay, Infection, Transfection, Control, Knockdown, Quantitative RT-PCR, Functional Assay, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Figure Lengend Snippet: TLR4 is the essential receptor mediating S100A8/A9-induced inflammation in HBE cells during K. pneumoniae infection. (A,B) HBE cells were pre-incubated with neutralizing antibodies against TLR4 (10 μg/mL), RAGE (100 μg/mL), or an isotype control (Iso Ctrl) for 1 h, followed by stimulation with recombinant human S100A8/A9 (20 μg/mL) for 24 h. Levels of (A) IL-8 and (B) IL-6 in supernatants were determined by ELISA. (C,D) HBE cells were pre-treated with the indicated antibodies for 1 h and subsequently infected with WT K. pneumoniae (MOI 100) for 24 h. Secretion of (C) IL-8 and (D) IL-6 was quantified by ELISA. All results are expressed as mean ± SEM of three independent experiments. * p < 0.05 compared with the indicated groups.

Techniques: Infection, Incubation, Control, Recombinant, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Figure Lengend Snippet: The S100A8/A9 autocrine loop drives NF-κB activation and subsequent cytokine release in HBE cells. (A) Representative immunoblots showing degradation of IκBα in primary HBE cells stimulated with rS100A8/A9 (20 μg/mL) for 60 min. β-Actin served as a loading control. (B) Densitometric quantification of IκBα protein levels from (A) . (C) Representative immunofluorescence images showing subcellular localization of the p65 subunit (green) at 60 min post-stimulation with rS100A8/A9. Nuclei were counterstained with DAPI (blue). (D) HBE cells were transfected with control siRNA (siCtrl) or siRNA targeting S100A9 (siS100A9) and subsequently infected with wild-type K. pneumoniae (MOI 100). Representative immunoblots of IκBα levels are shown at 60 min post-infection. (E) Densitometric quantification of IκBα degradation from (D) . (F) Representative immunofluorescence images showing p65 localization (green) in siCtrl- or siS100A9-transfected HBE cells at 60 min post- K. pneumoniae infection. Nuclei were stained with DAPI (blue). (G) Secretion of IL-8 and IL-6 by HBE cells. Cells were pre-treated with or without the NF-κB inhibitor BAY 11–7,082 (10 μM) for 60 min, followed by stimulation with rS100A8/A9 (20 μg/mL) for 24 h. Cytokine levels in supernatants were measured by ELISA. All graphs display mean ± SEM, * p < 0.05 compared with the untreated control (B,E,G) ; # p < 0.05 compared with siCtrl + Kp or the S100A8/A9-stimulated group without inhibitor (E,G) .

Techniques: Activation Assay, Western Blot, Control, Immunofluorescence, Transfection, Infection, Staining, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Figure Lengend Snippet: The epithelial S100A8/A9 autocrine loop is a critical driver of neutrophil chemotaxis in response to K. pneumoniae infection. Neutrophil chemotaxis was assessed using a Transwell assay. (A) Comparison of the chemotactic activity of supernatants from uninfected HBE cells (conditioned medium, CM), HBE cells infected with WT K. pneumoniae (MOI 100), and fMLP (positive control) on primary human neutrophils. (B) Comparison of the chemotactic activity of supernatants from infected control (siCtrl) HBE cells versus infected S100A9-deficient (siS100A9) HBE cells. Flow cytometry was used to determine the absolute number of migrated neutrophils. Data are shown as mean ± SEM from three separate experiments. * p < 0.05 vs. uninfected CM, # p < 0.05 vs. Kp + siCtrl.

Techniques: Chemotaxis Assay, Infection, Transwell Assay, Comparison, Activity Assay, Positive Control, Control, Flow Cytometry

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Figure Lengend Snippet: Proposed model of the S100A8/A9-mediated autocrine amplification loop in human airway epithelial cells during K. pneumoniae infection. Initial recognition of encapsulated K. pneumoniae by the airway epithelium triggers a primary transcriptional response, leading to the synthesis and secretion of the alarmin S100A8/A9 and a simultaneous upregulation of its cognate receptor, TLR4. This dual mechanism creates a primed state within the epithelium. The endogenously produced S100A8/A9 then acts back on the enriched TLR4 receptors in an autocrine or paracrine manner, activating the canonical NF-κB signaling pathway (characterized by IκB degradation and p65 nuclear translocation). This positive feedback loop significantly magnifies the production of pro-inflammatory cytokines such as IL-6 and IL-8, ultimately orchestrating massive neutrophil recruitment and driving the hyper-inflammation observed in severe pneumonia. Created in BioRender [You (2026) https://BioRender.com/qo9szis ].

Techniques: Amplification, Infection, Produced, Translocation Assay

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Article Snippet: For S100A8/A9 stimulating experiment, cells were incubated with endotoxin-free recombinant human S100A8/A9 protein (R&D Systems) at the indicated concentrations for specified durations.

Techniques: Infection, Expressing, Mutagenesis, Quantitative RT-PCR, Control

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Techniques: Infection, Expressing, Quantitative RT-PCR, Western Blot, Recombinant, Enzyme-linked Immunosorbent Assay, Control

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Techniques: Derivative Assay, Infection, Transfection, Control, Knockdown, Quantitative RT-PCR, Functional Assay, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Techniques: Infection, Incubation, Control, Recombinant, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Techniques: Activation Assay, Western Blot, Control, Immunofluorescence, Transfection, Infection, Staining, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Techniques: Chemotaxis Assay, Infection, Transwell Assay, Comparison, Activity Assay, Positive Control, Control, Flow Cytometry

Journal: Frontiers in Microbiology

Article Title: Klebsiella pneumoniae infection induces an S100A8/A9-mediated autocrine loop in human airway epithelium to amplify inflammation

doi: 10.3389/fmicb.2026.1768140

Techniques: Amplification, Infection, Produced, Translocation 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: To assess the impact of S100a8/a9 receptor inhibition, the mice were intraperitoneally injected with either Resatorvid (3 mg/kg/day, MCE, Cat# HY-11109) or FPS-ZM1 (10 mg/kg/day, MCE, Cat# HY-19370) for 3 days post-CLP.

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

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 )

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

TP activation inhibits S100a8/a9 transcription via PKCδ/Stat1 signaling. a Venn diagram illustrating the transcription factors (TFs) predicted to regulate S100a8/a9 expression identified through SCENIC analysis and PROMO database screening. b Heatmap displaying the activity levels of 21 transcription factors in control and TP-deficient DCs. c Violin plots showing the mRNA expression levels of four TFs ( Rela , Stat1 , Stat5a , and Atf1 ) in control and TP-deficient DCs from scRNA-seq. d Quantification of Stat1 expression in DCs from TP flox/flox and TP flox/flox CD11c Cre mice ( n = 5 mice per group). e Efficiency of siRNA-mediated Stat1 knockdown in control and U-46619-treated DC2.4 cells ( n = 6 wells per group). Relative mRNA levels of S100a8 ( f ) and S100a9 ( g ) in control and U-46619-treated DC2.4 cells after Stat1 knockdown ( n = 6–8 wells per group). h Western blot analysis of Stat1 and phosphor-Stat1 in spleen DCs from TP flox/flox and TP flox/flox CD11c Cre mice after CLP challenge. Effects of SQ29548 ( i ) and U-46619 ( j ) on S100a8 and S100a9 expression in DCs. k Effects of fludarabine on S100a8 and S100a9 expression in DCs with or without U-46619 treatment. l Western blot analysis of PKCβ, phosphor-PKCβ, PKCδ, and phosphor-PKCδ in spleen DCs from TP flox/flox and TP flox/flox CD11c Cre mice after CLP challenge. m Effect of rottlerin on Stat1 phosphorylation in DCs with or without U-46619 treatment. n , o Coimmunoprecipitation analysis of the interaction of PKCδ with Stat1 in DCs. p Effects of U-73122 on PKCδ and Stat1 phosphorylation in DCs treated with or without U-46619. q Effects of YM-254890 on phosphorylated PKCδ and phosphorylated Stat1 levels in DCs treated with or without U-46619. r Schematic illustration summarizing the TP-mediated inhibition of S100a8/a9 transcription via the G αq /PKCδ/Stat1 signaling pathway (Created with BioRender.com). Statistical significance was evaluated by the Mann–Whitney U test ( d ) and two-way ANOVA followed by Tukey’s test for multiple comparisons ( e – g )

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 activation inhibits S100a8/a9 transcription via PKCδ/Stat1 signaling. a Venn diagram illustrating the transcription factors (TFs) predicted to regulate S100a8/a9 expression identified through SCENIC analysis and PROMO database screening. b Heatmap displaying the activity levels of 21 transcription factors in control and TP-deficient DCs. c Violin plots showing the mRNA expression levels of four TFs ( Rela , Stat1 , Stat5a , and Atf1 ) in control and TP-deficient DCs from scRNA-seq. d Quantification of Stat1 expression in DCs from TP flox/flox and TP flox/flox CD11c Cre mice ( n = 5 mice per group). e Efficiency of siRNA-mediated Stat1 knockdown in control and U-46619-treated DC2.4 cells ( n = 6 wells per group). Relative mRNA levels of S100a8 ( f ) and S100a9 ( g ) in control and U-46619-treated DC2.4 cells after Stat1 knockdown ( n = 6–8 wells per group). h Western blot analysis of Stat1 and phosphor-Stat1 in spleen DCs from TP flox/flox and TP flox/flox CD11c Cre mice after CLP challenge. Effects of SQ29548 ( i ) and U-46619 ( j ) on S100a8 and S100a9 expression in DCs. k Effects of fludarabine on S100a8 and S100a9 expression in DCs with or without U-46619 treatment. l Western blot analysis of PKCβ, phosphor-PKCβ, PKCδ, and phosphor-PKCδ in spleen DCs from TP flox/flox and TP flox/flox CD11c Cre mice after CLP challenge. m Effect of rottlerin on Stat1 phosphorylation in DCs with or without U-46619 treatment. n , o Coimmunoprecipitation analysis of the interaction of PKCδ with Stat1 in DCs. p Effects of U-73122 on PKCδ and Stat1 phosphorylation in DCs treated with or without U-46619. q Effects of YM-254890 on phosphorylated PKCδ and phosphorylated Stat1 levels in DCs treated with or without U-46619. r Schematic illustration summarizing the TP-mediated inhibition of S100a8/a9 transcription via the G αq /PKCδ/Stat1 signaling pathway (Created with BioRender.com). Statistical significance was evaluated by the Mann–Whitney U test ( d ) and two-way ANOVA followed by Tukey’s test for multiple comparisons ( e – g )

Techniques: Activation Assay, Expressing, Activity Assay, Control, Knockdown, Western Blot, Phospho-proteomics, Inhibition, MANN-WHITNEY

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s100a8 a9 heterodimer (R&D Systems)

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