| First Author | Freitas A | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 12 | Pages | 7846-54 |
| PubMed ID | 19494309 | Mgi Jnum | J:149288 |
| Mgi Id | MGI:3848265 | Doi | 10.4049/jimmunol.0803039 |
| Citation | Freitas A, et al. (2009) IL-17 receptor signaling is required to control polymicrobial sepsis. J Immunol 182(12):7846-54 |
| abstractText | Sepsis is a systemic inflammatory response resulting from the inability of the host to contain the infection locally. Previously, we demonstrated that during severe sepsis there is a marked failure of neutrophil migration to the infection site, which contributes to dissemination of infection, resulting in high mortality. IL-17 plays an important role in neutrophil recruitment. Herein, we investigated the role of IL-17R signaling in polymicrobial sepsis induced by cecal ligation and puncture (CLP). It was observed that IL-17R-deficient mice, subjected to CLP-induced non-severe sepsis, show reduced neutrophil recruitment into the peritoneal cavity, spread of infection, and increased systemic inflammatory response as compared with C57BL/6 littermates. As a consequence, the mice showed an increased mortality rate. The ability of IL-17 to induce neutrophil migration was demonstrated in vivo and in vitro. Beside its role in neutrophil recruitment to the infection focus, IL-17 enhanced the microbicidal activity of the migrating neutrophils by a mechanism dependent on NO. Therefore, IL-17 plays a critical role in host protection during polymicrobial sepsis. |
