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R&D Systems recombinant human s100a8 a9 protein

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) .

Recombinant Human S100a8 A9 Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 12 article reviews

recombinant human s100a8 a9 protein - by Bioz Stars, 2026-08

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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

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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: 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

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

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