tetano
Editor, Senior Moderator
J Med Virol. 2015 Mar 19. doi: 10.1002/jmv.24138. [Epub ahead of print]
[h=1]Induction of interleukin-1 beta (IL-1β) is a critical component of lung inflammation during influenza A (H1N1) virus infection.[/h] Kim KS[SUP]1[/SUP], Jung H, Shin IK, Choi BR, Kim DH.
[h=3]Author information[/h]
[h=3]Abstract[/h] 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. ? 2015 Wiley Periodicals, Inc.
? 2015 Wiley Periodicals, Inc.
[h=4]KEYWORDS:[/h] IL-1β; cytokine; endothelial cells; inflammation; influenza
PMID: 25802122 [PubMed - as supplied by publisher]
[h=1]Induction of interleukin-1 beta (IL-1β) is a critical component of lung inflammation during influenza A (H1N1) virus infection.[/h] Kim KS[SUP]1[/SUP], Jung H, Shin IK, Choi BR, Kim DH.
[h=3]Author information[/h]
[h=3]Abstract[/h] 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. ? 2015 Wiley Periodicals, Inc.
? 2015 Wiley Periodicals, Inc.
[h=4]KEYWORDS:[/h] IL-1β; cytokine; endothelial cells; inflammation; influenza
PMID: 25802122 [PubMed - as supplied by publisher]