ArticlePloS one2015
S100A9 induced inflammatory responses are mediated by distinct damage associated molecular patterns (DAMP) receptors in vitro and in vivo.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 125 citations in OpenAlex.
- Upregulation of S100A9 in orbital tissues of patients with thyroid eye disease.International ophthalmology · 2026Article
- Cytokine signalling in vaginal epithelial cells: mechanistic insights into epithelial immunity and inflammatory milieu in vulvovaginal candidiasis.European cytokine network · 2026Review
- RAGE-Mediated Signalling in Gynaecological Disorders: Review of Molecular Mechanisms and Therapeutic Perspectives.Expert reviews in molecular medicine · 2026Review
- Epidermal PPARγ Signaling as a Suppressor of Toll-like Receptor-Mediated Inflammation and Fibrosis: Relevance to Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- Cancer cachexia induces senescent reprogramming of brown adipose tissue and pro-cachectic S100A9 secretion by adipocytes.Cell death & disease · 2026Article
- Intestinal REG3G Protects Against Gastrointestinal Dysfunction in a Murine Model of Ethanol Intoxication and Burn Injury.Shock (Augusta, Ga.) · 2026Article
- Evaluation of salivary calprotectin as a marker for screening periodontitis using a latex agglutination turbidimetric immunoassay system: a cross-sectional study.BMC oral health · 2026Article
- Neutrophil-Endothelium Interaction Mediated by S100A9 Promotes Pulmonary Vascular Remodeling During Pulmonary Hypertension.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Shared blood gene signature in lung adenocarcinoma and microbial lung infections: a bioinformatic analysis and in silico validation.Discover oncology · 2025Article
- Hypoxia-Induced Metabolic Reprogramming and Markings of Cell Fate in Concentric Arterial Hypertrophy.bioRxiv : the preprint server for biology · 2025Article
- Diclofenac Immune-Mediated Hepatitis: Identification of Innate and Adaptive Immune Responses at Clinically Relevant Doses.International journal of molecular sciences · 2025Article
- Virtual Probing on the Influence of CaCell biochemistry and biophysics · 2025Article
- Life-threatening risk factors contribute to the development of diseases with the highest mortality through the induction of regulated necrotic cell death.Cell death & disease · 2025Review
- Extracellular vesicle-bound S100A8/A9 is differentially expressed in septic shock and prompts acute lung injury.Respiratory research · 2025Article
- The presence of glutathione S-transferase in recombinant S100A9 alters its effect on human sperm function.Journal of biomedical research · 2025Article
- Zebrafish do not have a calprotectin ortholog.PloS one · 2025Article
- Reducing the excessive inflammation after burn injury in aged mice by maintaining a healthier intestinal microbiome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Changing expression system alters oligomerization and proinflammatory activity of recombinant human S100A9.bioRxiv : the preprint server for biology · 2024Article
- Data-independent LC-MS/MS analysis of ME/CFS plasma reveals a dysregulated coagulation system, endothelial dysfunction, downregulation of complement machinery.Cardiovascular diabetology · 2024Article
- S100A9: The Unusual Suspect Connecting Viral Infection and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Release of endogenous damage associated molecular patterns (DAMPs), including members of the S100 family, are associated with infection, cellular stress, tissue damage and cancer. The extracellular functions of this family of calcium binding proteins, particularly S100A8, S100A9 and S100A12, are being delineated. They appear to mediate their functions via receptor for advanced glycation endproducts (RAGE) or TLR4, but there remains considerable uncertainty over the relative physiological roles of these DAMPs and their pattern recognition receptors. In this study, we surveyed the capacity of S100 proteins to induce proinflammatory cytokines and cell migration, and the contribution RAGE and TLR4 to mediate these responses in vitro. Using adenoviral delivery of murine S100A9, we also examined the potential for S100A9 homodimers to trigger lung inflammation in vivo. S100A8, S100A9 and S100A12, but not the S100A8/A9 heterodimer, induced modest levels of TLR4-mediated cytokine production from human PBMC. In contrast, for most S100s including S100A9, RAGE blockade inhibited S100-mediated cell migration of THP1 cells and major leukocyte populations, whereas TLR4-blockade had no effect. Intranasal administration of murine S100A9 adenovirus induced a specific, time-dependent predominately macrophage infiltration that coincided with elevated S100A9 levels and proinflammatory cytokines in the BAL fluid. Inflammatory cytokines were markedly ablated in the TLR4-defective mice, but unexpectedly the loss of TLR4 signaling or RAGE-deficiency did not appreciably impact the S100A9-mediated lung pathology or the inflammatory cell infiltrate in the alveolar space. These data demonstrate that physiological levels of S100A9 homodimers can trigger an inflammatory response in vivo, and despite the capacity of RAGE and TLR4 blockade to inhibit responses in vitro, the response is predominately independent of both these receptors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.