| First Author | Auerbuch V | Year | 2004 |
| Journal | J Exp Med | Volume | 200 |
| Issue | 4 | Pages | 527-33 |
| PubMed ID | 15302899 | Mgi Jnum | J:93932 |
| Mgi Id | MGI:3510281 | Doi | 10.1084/jem.20040976 |
| Citation | Auerbuch V, et al. (2004) Mice lacking the type I interferon receptor are resistant to Listeria monocytogenes. J Exp Med 200(4):527-33 |
| abstractText | Listeria monocytogenes is a facultative intracellular pathogen that induces a cytosolic signaling cascade resulting in expression of interferon (IFN)-beta. Although type I IFNs are critical in viral defense, their role in immunity to bacterial pathogens is much less clear. In this study, we addressed the role of type I IFNs by examining the infection of L. monocytogenes in BALB/c mice lacking the type I IFN receptor (IFN-alpha/betaR-/-). During the first 24 h of infection in vivo, IFN-alpha/betaR-/- and wild-type mice were similar in terms of L. monocytogenes survival. In addition, the intracellular fate of L. monocytogenes in macrophages cultured from IFN-alpha/betaR-/- and wild-type mice was indistinguishable. However, by 72 h after inoculation in vivo, IFN-alpha/betaR-/- mice were approximately 1,000-fold more resistant to a high dose L. monocytogenes infection. Resistance was correlated with elevated levels of interleukin 12p70 in the blood and increased numbers of CD11b+ macrophages producing tumor necrosis factor alpha in the spleen of IFN-alpha/betaR-/- mice. The results of this study suggest that L. monocytogenes might be exploiting an innate antiviral response to promote its pathogenesis. |
