The Effect of Nipah Virus-Induced Oxidative Stress on the Immune Response in Human Airway Epithelial Cells
Year: 2016
Type: article
Abstract: Nipah virus (NiV) is a deadly agent of the family Paramyxoviridae that can cause in humans a severe pneumonia, resulting in acute lung injury and inflammation of the small airways. Interestingly, Reactive Oxygen Species (ROS) produced by airway epithelial cells in response to other paramyxovirus infection contribute to the pathogenesis of lung inflammation by inducing pro-inflammatory gene expression and oxidative stress. However, the cellular mechanisms involved in NiV-induced lung inflammation remain unclear. Here, we investigated whether NiV-infected human airway epithelial cells undergo oxidative stress and its role in inflammation modulation. The Nrf2-mediated oxidative stress pathway was significantly affected during infection. Oxidative stress was confirmed in infected cells using the isoprostane marker and by monitoring the GSH/GSSG ratio, which correlated with reduction of antioxidant enzyme expression. Interestingly, treatment of infected cells with antioxidants resulted in a dose-dependent decrease of isoprostane and the pro-inflammatory response. BHA also lowered virus replication. These results suggest that oxidative stress in NiV-infected respiratory epithelium is caused by inefficient ROS decomposition, due to insufficiency of antioxidant enzymes, and modulate inflammation. Oxidative stress was further confirmed in NiV-infected human lung xenografts demonstrating the relevance of such phenomenon in vivo. Managing ROS levels might be part of the treatment.
Language: English
Topic: Virology and Viral Diseases
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2506258342