| First Author | Gao JL | Year | 1999 |
| Journal | J Exp Med | Volume | 189 |
| Issue | 4 | Pages | 657-62 |
| PubMed ID | 9989980 | Mgi Jnum | J:53354 |
| Mgi Id | MGI:1332336 | Doi | 10.1084/jem.189.4.657 |
| Citation | Gao JL, et al. (1999) Impaired antibacterial host defense in mice lacking the N-formylpeptide receptor. J Exp Med 189(4):657-62 |
| abstractText | N-formylpeptides derive from bacterial and mitochondrial proteins, and bind to specific receptors on mammalian phagocytes. Since binding induces chemotaxis and activation of phagocytes in vitro, it has been postulated that N-formylpeptide receptor signaling in vivo may be important in antimicrobial host defense, although direct proof has been lacking. Here we test this hypothesis in mice lacking the high affinity N-formylpeptide receptor (FPR), created by targeted gene disruption. FPR-/- mice developed normally, but had increased susceptibility to challenge with Listeria monocytogenes, as measured by increased mortality compared with wild-type littermates. FPR-/- mice also had increased bacterial load in spleen and liver 2 d after infection, which is before development of a specific cellular immune response, suggesting a defect in innate immunity. Consistent with this, neutrophil chemotaxis in vitro and neutrophil mobilization into peripheral blood in vivo in response to the prototype N-formylpeptide fMLF (formyl-methionyl-leucyl-phenylalanine) were both absent in FPR-/- mice. These results indicate that FPR functions in antibacterial host defense in vivo. |
