期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 200, 期 4, 页码 527-533出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20040976
关键词
TNF-alpha; CD11b antigen; macrophage; IL-12; pathogen
资金
- NIAID NIH HHS [R37 AI029619, R01 AI27655, R01 AI29619, R01 AI027655] Funding Source: Medline
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 similar to1,000-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.
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