Induction of interleukin-1 beta (IL-1β) is a critical component of lung inflammation during influenza A (H1N1) virus infection.

Cytokine storm during influenza virus infection is recognized as a predictor of morbidity and mortality. To verify the cellular effects of influenza-induced cytokines in primary normal lung cells, human pulmonary microvascular endothelial cells (HMVECs) and lung fibroblast cells (MRC-5 cells) were infected with influenza virus H1N1. H1N1 infection induced the transcription of various genes encoding cytokines and chemokines such as interleukin-1 beta (IL-1β), IL-6, IL-8, IL-12A, tumor necrosis factor alpha (TNF-α), and chemokine (C-C motif) ligand 5 (CCL5) in both endothelial cells and lung fibroblasts. Among them, IL-1β induction by influenza infection increased the inflammation of lung cells; conversely, blockade of IL-1β signals with an IL-1β receptor antagonist or a neutralizing antibody alleviated influenza-driven inflammation. In conclusion, these data suggest that secreted IL-1β by the endothelial cells contributes to influenza-induced inflammation, and blockade of IL-1β signals is a potential treatment or therapeutic target for influenza-induced inflammation.