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- W4313360257 abstract "Abstract Staphylococcus aureus has emerged as a leading contributor to morbidity and mortality during recent influenza pandemics and epidemics. The mechanism for this influenza-induced susceptibility to secondary bacterial infection is incompletely understood. We have previously reported that innate antibacterial immunity is suppressed during the recovery stage of influenza infection. This impairment of bacterial control coincides with airway accumulation of inflammatory monocytes, and therefore, we investigated in this study a novel hypothesis of influenza-induced suppression of antibacterial immunity: recruitment of monocytes. C-C chemokine receptor type 2 (CCR2) is responsible for the recruitment of Ly6C+ monocytes into lungs after influenza infection. Here we demonstrate that CCR2−/− mice were more resistant than wild-type mice to influenza and S. aureus coinfection. CCR2 deficiency not only resulted in diminished monocyte recruitment but also reduced proinflammatory cytokine response to coinfection. Importantly, despite a delay in viral clearance, CCR2−/− mice exhibited significantly improved lung bacterial control, in agreement with their increased survivals from influenza and S. aureus coinfection. Furthermore, we show that CCR2-recruited monocytes served as reservoirs to protect bacteria from killing by antibiotics and more potent neutrophils. Collectively, our findings indicate that inflammatory monocytes constitute an important and hitherto underappreciated mechanism of the conflicting immune requirements for viral versus bacterial control by hosts, which subsequently leads to the worsen outcome of influenza and S. aureus coinfection." @default.
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- W4313360257 date "2017-05-01" @default.
- W4313360257 modified "2023-09-26" @default.
- W4313360257 title "Recruitment of inflammatory monocytes during influenza infection predisposes host to secondary <i>S. aureus</i> infection" @default.
- W4313360257 doi "https://doi.org/10.4049/jimmunol.198.supp.68.3" @default.
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