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The Journal of Immunology, 2004, 172: 20-24.
Copyright © 2004 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: An Endogenous Pathway to Systemic Inflammatory Response Syndrome (SIRS)-Like Reactions through Toll-Like Receptor 41

Geoffrey B. Johnson*, Gregory J. Brunn{dagger} and Jeffrey L. Platt2,*,{dagger},{ddagger},§

Departments of * Immunology, {dagger} Pharmacology and Experimental Therapeutics, {ddagger} Surgery, and § Pediatrics, Mayo Clinic, Rochester, MN 55905

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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