| First Author | Wang F | Year | 2012 |
| Journal | Cell Immunol | Volume | 272 |
| Issue | 2 | Pages | 251-8 |
| PubMed ID | 22055202 | Mgi Jnum | J:181381 |
| Mgi Id | MGI:5311105 | Doi | 10.1016/j.cellimm.2011.10.006 |
| Citation | Wang F, et al. (2012) Blocking TREM-1 signaling prolongs survival of mice with Pseudomonas aeruginosa induced sepsis. Cell Immunol 272(2):251-8 |
| abstractText | TREM-1 is a recently discovered receptor expressed on neutrophils and macrophages. Blocking of TREM-1 signaling improves the survival of mice with bacterial sepsis. However, the precise mechanism by which TREM-1 modulates the inflammatory responses is poorly defined. In this study, we investigated the role of TREM-1 in Pseudomonas aeruginosa-induced peritonitis. Our results showed that TREM-1 was not expressed on lymphocytes but emerged on the cell surface of neutrophils and peritoneal macrophages. Blockade of TREM-1 signaling significantly prolonged survival of mice with P. aeruginosa-induced peritonitis. However, blocking TREM-1 signaling had no effect on macrophage phagocytosis in vitro. Interestingly, the expression of the costimulatory molecules CD40 and CD86 on macrophages was significantly decreased after blocking TREM-1 signaling. Furthermore, interfering with TREM-1 engagement led to significant reduction of pro-inflammatory mediators such as IL-1, TNF-alpha, MCP-1 and IFN-gamma. Therefore, our results showed that TREM-1 could be a potential therapeutic target for bacterial sepsis. |
