Cutting Edge: An Endogenous Pathway to Systemic Inflammatory Response Syndrome (SIRS)-Like Reactions through Toll-Like Receptor 4
| Autor: | Jeffrey L. Platt, Gregory J. Brunn, Geoffrey B. Johnson |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Swine
Immunology Receptors Cell Surface Biology Sepsis Mice chemistry.chemical_compound medicine Animals Immunology and Allergy Receptor Pancreatic elastase Cells Cultured Mice Knockout Mice Inbred C3H Toll-like receptor Membrane Glycoproteins Pancreatic Elastase Tumor Necrosis Factor-alpha Toll-Like Receptors Elastase Injections Intralymphatic Heparan sulfate medicine.disease Coculture Techniques Systemic Inflammatory Response Syndrome humanities Mice Inbred C57BL Systemic inflammatory response syndrome Solubility chemistry Female Heparitin Sulfate Signal transduction Heparan Sulfate Proteoglycans Injections Intraperitoneal Spleen Signal Transduction |
| Zdroj: | The Journal of Immunology. 172:20-24 |
| ISSN: | 1550-6606 0022-1767 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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