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- W2954392110 endingPage "105710" @default.
- W2954392110 startingPage "105710" @default.
- W2954392110 abstract "Type I interferon (IFN) is indispensable for antiviral immunity, but its role in bacterial infections is controversial and not fully described. Nontypeable Haemophilus influenzae (NTHi) is one of the most common bacterial pathogens in patients with chronic obstructive pulmonary disease (COPD). NTHi-DNA activates type I IFN production in macrophages, but the function of type I IFN in host-pathogen interactions, in the context of NTHi infection, is still unclear. Here, we showed that type I IFN, induced by NTHi-DNA, restrained bacterial killing in vitro and promoted COPD development in vivo in response to NTHi. Mice deficient for type I IFN receptor (IFNAR) exhibited improved resistance to NTHi infection. Moreover, similar to exogenous IFN-β, NTHi-DNA-induced type I IFN increased the production of IL-6, IL-1β, IL-12 and CXCL10 via p38 MAPK activation. Our findings demonstrated that NTHi-DNA-induced type I IFN signaling played a negative role in host defense against NTHi infection and identified potential targets for future therapeutic management of COPD." @default.
- W2954392110 created "2019-07-12" @default.
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- W2954392110 date "2019-09-01" @default.
- W2954392110 modified "2023-09-25" @default.
- W2954392110 title "Type I interferon induced by DNA of nontypeable Haemophilus influenza modulates inflammatory cytokine profile to promote susceptibility to this bacterium" @default.
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- W2954392110 doi "https://doi.org/10.1016/j.intimp.2019.105710" @default.
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