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

Abstract

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.

Protective effects of phillyrin against influenza A virus in vivo

“…Influenza virus infection may cause inflammation, lung lesions and injury. Early lung inflammation and excessive early cytokine responses are key contributors to the high morbidity and mortality associated with influenza infection (Iwasaki and Medzhitov 2011;Kim et al 2015;Oldstone and Rosen 2014;Price et al 2015;Woo et al 2010). Our results showed that phillyrin could decrease the lung index and attenuate lung tissue damage.…”

Viral interference between low pathogenic avian influenza H9N2 and avian infectious bronchitis viruses in vitro and in ovo

“…Nil and colleagues reported that expression of pro-inflammatory cytokines (IL-1 beta and IL-6) was higher in IBV infected group than in control group, suggesting that these are involved in IBV progression as they are expressed in response to viral infection, and constituting another mode of resistance of the organism (Nil et al, 2014). IL-1β was reported to be the central cytokine that accompanies inflammation, as it is implicated in promoting pulmonary tissue pathology (Kim et al, 2015). The ELISA results showed important secretion of IL-1β in CEL cells following dual infection, which could explain the interference between AIV and IBV.…”

“…A general antiviral response is generated through the activation of a broad range of effectors molecules, including myxovirus resistance gene I, RNA-activated protein kinase and 2′,5′-oligoadenylate synthetases (Daviet et al, 2009;Garcia-Sastre, 2001). IL-1β expression is induced by toll like receptors that warrant its presence early after viral infection of chickens (Jianlin et al, 2016;Kim et al, 2015).…”

Fibroblast growth factor 23 and Klotho contribute to airway inflammation

“…Since cigarette smoke downregulates klotho expression, FGF23 signaling occurs via FGFR4 as we have previously demonstrated in the liver and in the myocardium (17,18). This ultimately leads to an increase in IL-1β secretion, a key cytokine in virus-induced lung disease (31). Administration of an IL-1β antibody reduces lung inflammation in a mouse model of influenza (32).…”