| First Author | Nagamatsu K | Year | 2009 |
| Journal | J Exp Med | Volume | 206 |
| Issue | 13 | Pages | 3073-88 |
| PubMed ID | 20008527 | Mgi Jnum | J:155669 |
| Mgi Id | MGI:4415079 | Doi | 10.1084/jem.20090494 |
| Citation | Nagamatsu K, et al. (2009) Bordetella evades the host immune system by inducing IL-10 through a type III effector, BopN. J Exp Med 206(13):3073-88 |
| abstractText | The inflammatory response is one of several host alert mechanisms that recruit neutrophils from the circulation to the area of infection. We demonstrate that Bordetella, a bacterial pathogen, exploits an antiinflammatory cytokine, interleukin-10 (IL-10), to evade the host immune system. We identified a Bordetella effector, BopN, that is translocated into the host cell via the type III secretion system, where it induces enhanced production of IL-10. Interestingly, the BopN effector translocates itself into the nucleus and is involved in the down-regulation of mitogen-activated protein kinases. Using pharmacological blockade, we demonstrated that BopN-induced IL-10 production is mediated, at least in part, by its ability to block the extracellular signal-regulated kinase pathway. We also showed that BopN blocks nuclear translocation of nuclear factor kappaB p65 (NF-kappaBp65) but, in contrast, promotes nuclear translocation of NF-kappaBp50. A BopN-deficient strain was unable to induce IL-10 production in mice, resulting in the elimination of bacteria via neutrophil infiltration into the pulmonary alveoli. Furthermore, IL-10-deficient mice effectively eliminated wild-type as well as BopN mutant bacteria. Thus, Bordetella exploits BopN as a stealth strategy to shut off the host inflammatory reaction. These results explain the ability of Bordetella species to avoid induction of the inflammatory response. |
