Journal
JOURNAL OF IMMUNOLOGY
Volume 172, Issue 1, Pages 20-24Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.1.20
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL046810] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI053733] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL 46810] Funding Source: Medline
- NIAID NIH HHS [AI 53733] Funding Source: Medline
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Systemic inflammatory response syndrome (SIRS) is typically associated with trauma, surgery, or acute pancreatitis. SIRS resembles sepsis, triggered by exogenous macromolecules such as LPS acting on Toll-like receptors. What triggers SIRS in the absence of infection, however, is unknown. In this study, we report that a SIRS-like response can be induced in mice by administration of soluble heparan sulfate, a glycosaminoglycan associated with nucleated cells and extracellular matrices, and by elastase, which cleaves and releases heparan sulfate proteoglycans. The ability of heparan sulfate and elastase to induce SIRS depends on functional Toll-like receptor 4, because mutant mice lacking that receptor or its function do not respond. These results provide a molecular explanation for the initiation of SIRS.
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