期刊
CELL REPORTS
卷 22, 期 12, 页码 3168-3174出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.02.096
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资金
- NIH [AI101935, AI124346, AR056296, CA163507]
- American Lebanese Syrian Associated Charities
- R.G. Menzies Early Career Fellowship from the National Health and Medical Research Council of Australia
- NATIONAL CANCER INSTITUTE [P30CA021765, R01CA163507] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI101935, R01AI124346, R37AI101935] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR056296] Funding Source: NIH RePORTER
Interferons (IFNs) and inflammasomes are essential mediators of anti-microbial immunity. Type I IFN signaling drives activation of the AIM2 inflammasome in macrophages; however, the relative contribution of IFNs and inflammasome responses in host defense is less understood. We report intact AIM2 inflammasome responses in mice lacking type I IFN signaling during infection with F. novicida. Lack of type I IFN signaling conferred protection to F. novicida infection in contrast to the increased susceptibility in AIM2-deficient mice. Mice lacking both AIM2 and IFNAR2 were protected against the infection. The detrimental effects of type I IFN signaling were due to its ability to induce activation of apoptotic caspases and cell death. These results demonstrate the contrasting effects of type I IFN signaling and AIM2 during F. novicida infection in vivo and indicate a dominant role for type I IFNs in mediating detrimental responses despite the protective AIM2 inflammasome responses.
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