期刊
SCIENCE
卷 340, 期 6137, 页码 1230-1234出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1233632
关键词
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资金
- Howard Hughes Medical Institute
- NIH [R01 046688, AI R01 055502]
- Ellison Foundation
- New England Regional Center of Excellence
- FWF (Austrian Science Fund) [P25235-B13]
- Austrian Science Fund (FWF) [P 25235] Funding Source: researchfish
- Austrian Science Fund (FWF) [P25235] Funding Source: Austrian Science Fund (FWF)
Secondary bacterial pneumonia leads to increased morbidity and mortality from influenza virus infections. What causes this increased susceptibility, however, is not well defined. Host defense from infection relies not only on immune resistance mechanisms but also on the ability to tolerate a given level of pathogen burden. Failure of either resistance or tolerance can contribute to disease severity, making it hard to distinguish their relative contribution. We employ a coinfection mouse model of influenza virus and Legionella pneumophila in which we can separate resistance and tolerance. We demonstrate that influenza virus can promote susceptibility to lethal bacterial coinfection, even when bacterial infection is controlled by the immune system. We propose that this failure of host defense is due to impaired ability to tolerate tissue damage.
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