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Induction of interleukin‐1 beta (IL‐1β) is a critical component of lung inflammation during influenza A (H1N1) virus infection
Author(s) -
Kim Kwang Seok,
Jung Hyemin,
Shin In Kyung,
Choi BoRa,
Kim Dong Ho
Publication year - 2015
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.24138
Subject(s) - virology , virus , immunology , influenza a virus , inflammation , beta (programming language) , medicine , lung , interleukin , biology , cytokine , computer science , programming language
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. J. Med. Virol. 87:1104–1112, 2015 . © 2015 Wiley Periodicals, Inc.