期刊
SCIENCE
卷 363, 期 6434, 页码 1416-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aat9691
关键词
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资金
- Stanford SPARK [R21AI133370, R21AI133240, R01AI12492093]
- Falk Medical Research Trust
- Cystic Fibrosis Foundation (CFF)
- Gabilan Stanford Graduate Fellowship for Science and Engineering
- Lubert Stryer Bio-X Stanford Interdisciplinary Graduate Fellowship
- NIH [K22AI125282, R01AI138981, P20GM103546, R01GM111808]
- Stanford Diabetes Research Center (SDRC) [P30DK116074]
- ARRA award [1S10RR026780-F Resources]
Bacteriophage are abundant at sites of bacterial infection, but their effects on mammalian hosts are unclear. We have identified pathogenic roles for filamentous Pf bacteriophage produced by Pseudomonas aeruginosa (Pa) in suppression of immunity against bacterial infection. Pf promote Pa wound infection in mice and are associated with chronic human Pa wound infections. Murine and human leukocytes endocytose Pf, and internalization of this single-stranded DNA virus results in phage RNA production. This triggers Toll-like receptor 3 (TLR3)- and TIR domain-containing adapter-inducing interferon-beta (TRIF)-dependent type I interferon production, inhibition of tumor necrosis factor (TNF), and the suppression of phagocytosis. Conversely, immunization of mice against Pf prevents Pa wound infection. Thus, Pf triggers maladaptive innate viral pattern-recognition responses, which impair bacterial clearance. Vaccination against phage virions represents a potential strategy to prevent bacterial infection.
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