| First Author | Wen H | Year | 2007 |
| Journal | Eur J Immunol | Volume | 37 |
| Issue | 9 | Pages | 2487-98 |
| PubMed ID | 17694574 | Mgi Jnum | J:124358 |
| Mgi Id | MGI:3721367 | Doi | 10.1002/eji.200737370 |
| Citation | Wen H, et al. (2007) The chemokine receptor CCR6 is an important component of the innate immune response. Eur J Immunol 37(9):2487-98 |
| abstractText | In our initial studies we found that naive CCR6-deficient (CCR6(-/-)) C57BL/6 mice possessed significantly lower number of both F4/80(+) macrophages and dendritic cells (DC), but higher number of B cells in the peritoneal cavity, as compared to naive wild type (WT) controls. Furthermore, peritoneal macrophages isolated from CCR6(-/-) mice expressed significantly lower levels of inflammatory cytokines and nitric oxide following lipopolysaccharide (LPS)stimulation, as compared to WT macrophages. In a severe experimental peritonitis model induced by cecal ligation and puncture (CLP), CCR6(-/-) mice were protected when compared with WT controls. At 24 h following the induction of peritonitis, CCR6(-/-) mice exhibited significantly lower levels of inflammatory cytokines/chemokines in both the peritoneal cavity and blood. Interestingly, DC recruitment into the peritoneal cavity was impaired in CCR6(-/-) mice during the evolution of CLP-induced peritonitis. Peritoneal macrophages isolated from surviving CCR6(-/-) mice 3 days after CLP-induced peritonitis exhibited an enhanced LPS response compared with similarly treated WT peritoneal macrophages. These data illustrate that CCR6 deficiency alters the innate response via attenuating the hyperactive local and systemic inflammatory response during CLP-induced peritonitis. |
