期刊
JOURNAL OF IMMUNOLOGY
卷 181, 期 12, 页码 8194-8198出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.12.8194
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资金
- National Institutes of Health [AI063331, AI064748]
- Jung-Stiftung fur Wissenschaft und Forschung
- German Research Foundation (Deutsche Forschungsgemeinschaft)
- Heisenberg-Stipendium of the Deutsche Forschungsgemeinschah
Endogenous danger signals released from necrotic cells are thought to be sensed by phagocytes leading to secretion of IL-1 alpha and neutrophilic recruitment. However, the mechanisms for IL-1 alpha production and IL-1 alpha-mediated sterile inflammation remain poorly understood. We report here that necrotic cell extracts elicited little secretion of CXCL1 and IL-6 from macrophages but robust production in mesothelial cells. The induction of CXCL1 as well as activation of NF-kappa B and MAPKs by cytosolic extracts required the presence of IL-1a in the necrotic cell. Conversely, expression of IL-1R and MyD88 but not IL-1 alpha, RICK, TLR2, TLR4, TRIF, or inflammasome components in mesothelial cells was critical for the production of CXCL1. Furthermore, IL-1 alpha was critical to induce the recruitment of neutrophils in the peritoneal cavity via CXCR2. These studies show that IL-1 alpha is a key danger signal released from necrotic cells to trigger CXCL1 secretion and recruitment of neutrophils via IL-1R/MyD88 on neighboring mesothelial cells. The Journal of Immunology, 2008, 181: 8194-8198.
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