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Significance Influenza A virus (IAV) infection poses a significant challenge to public health. The cellular and molecular mechanisms regulating the development of excessive pulmonary inflammation following IAV infection remain largely undefined. We find that the loss of BCL6 in neutrophils mitigates lung inflammation and promotes host resistance to IAV infection. The data provide mechanistic insight into how BCL6 regulates neutrophil-mediated lung inflammation through modulating neutrophil apoptosis at the site of IAV infection. Thus, targeting neutrophil survival in the tissue may be a promising therapeutic option to decrease host inflammation and minimize lung injury for severe IAV infection.

BCL6 modulates tissue neutrophil survival and exacerbates pulmonary inflammation following influenza virus infection