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Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface
Published on: October 8, 2013
Exposure to PM2.5 modulate the pro-inflammatory and interferon responses against influenza virus infection in a human
Chloé Chivé1, Lydie Martίn-Faivre2, Alice Eon-Bertho3
1Université Paris Cité, Functional and Adaptive Biology Unit, UMR8251-CNRS, Paris, France; French Environment and Energy Management Agency 20, Avenue Du Grésillé - BP, 90406 49004, Angers, France.
Abstract:
Epidemiological studies showed a positive association between exposure to PM2.5 and the severity of influenza virus infection. However, the mechanisms by which PM2.5 can disrupt antiviral defence are still unclear. From this perspective, the objective of this study was to evaluate the effects of PM2.5 on antiviral signalling in the respiratory epithelium using the bronchial Calu-3 cell line grown at the air-liquid interface. Pre-exposure to PM2.5 before infection with the influenza virus was investigated, as well as a co-exposure. Although a physical interaction between the virus and the particles seems possible, no effect of PM2.5 on viral replication was observed during co-exposure, although a downregulation of IFN-β release was associated to PM2.5 exposure. However, pre-exposure slightly increased the viral nucleoprotein production and the pro-inflammatory response. Conversely, the level of the myxovirus resistance protein A (MxA), an interferon-stimulated gene (ISG) induced by IFN-β, was reduced. Therefore, these results suggest that pre-exposure to PM2.5 could alter the antiviral response of bronchial epithelial cells, increasing their susceptibility to viral infection.
Insights
Exposure to fine particulate matter (PM2.5) may weaken respiratory cells' defense against influenza. Pre-exposure to PM2.5 reduced antiviral responses, potentially increasing susceptibility to viral infections.
Area of Science:
- Environmental Health
- Virology
- Cell Biology
Background:
- Epidemiological studies link fine particulate matter (PM2.5) exposure to increased influenza severity.
- The precise mechanisms by which PM2.5 compromises antiviral defenses remain largely unknown.
Purpose of the Study:
- To investigate the impact of PM2.5 on antiviral signaling pathways in human bronchial epithelial cells (Calu-3) at the air-liquid interface.
- To differentiate the effects of PM2.5 pre-exposure versus co-exposure on influenza virus infection.
Main Methods:
- Utilized the Calu-3 bronchial cell line cultured at an air-liquid interface to model respiratory epithelium.
- Exposed cells to PM2.5 either before (pre-exposure) or during (co-exposure) influenza virus infection.
- Assessed viral replication, interferon-beta (IFN-β) release, pro-inflammatory cytokine production, and the expression of interferon-stimulated genes like myxovirus resistance protein A (MxA).
Main Results:
- Co-exposure to PM2.5 did not affect viral replication but was associated with reduced IFN-β release.
- Pre-exposure to PM2.5 led to increased viral nucleoprotein production and a heightened pro-inflammatory response.
- Pre-exposure to PM2.5 significantly decreased MxA levels, an important antiviral protein induced by IFN-β.
Conclusions:
- Pre-exposure to PM2.5 appears to impair the innate antiviral defense mechanisms in bronchial epithelial cells.
- These alterations may render the respiratory epithelium more vulnerable to influenza virus infection.
- PM2.5-induced disruption of antiviral signaling is a critical factor in understanding its role in respiratory viral disease severity.
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