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Influenza-related pneumonia is an important complication of influenza, and it has been suggested that excessive inflammatory reactions, including “cytokine storm”, may contribute to the mechanisms underlying severe pneumonia. Human data and mice co-infected with influenza virus and Streptococcus pneumoniae show increased severity of illness according to the elevation of cytokines/chemokines, and mice with genetic knock-out of immune molecules such as Toll-like receptor 3 and IRAK-M also show hyper-immune responses and reduced survival following influenza virus infection. Such findings suggest that innate immune responses and excessive neutrophil activation might be related to severe inflammatory changes in the lungs, and immunomudulatory therapy may thus be effective against severe influenza-related pneumonia.
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