tetano
Editor, Senior Moderator
Environ Pollut
. 2024 Mar 14:123781.
doi: 10.1016/j.envpol.2024.123781. Online ahead of print. Exposure to PM[SUB]2.5[/SUB] modulate the pro-inflammatory and interferon responses against influenza virus infection in a human 3D bronchial epithelium model
Chloé Chivé[SUP] 1 [/SUP], Lydie Martίn-Faivre[SUP] 2 [/SUP], Alice Eon-Bertho[SUP] 3 [/SUP], Christelle Alwardini[SUP] 3 [/SUP], Jéril Degrouard[SUP] 4 [/SUP], Alexandre Albinet[SUP] 5 [/SUP], Gael Noyalet[SUP] 6 [/SUP], Servanne Chevaillier[SUP] 6 [/SUP], Franck Maisonneuve[SUP] 7 [/SUP], Jean-Michel Sallenave[SUP] 2 [/SUP], Stéphanie Devineau[SUP] 3 [/SUP], Vincent Michoud[SUP] 6 [/SUP], Ignacio Garcia-Verdugo[SUP] 8 [/SUP], Armelle Baeza-Squiban[SUP] 3 [/SUP]
Affiliations
Epidemiological studies showed a positive association between exposure to PM[SUB]2.5[/SUB] and the severity of influenza virus infection. However, the mechanisms by which PM[SUB]2.5[/SUB] can disrupt antiviral defence are still unclear. From this perspective, the objective of this study was to evaluate the effects of PM[SUB]2.5[/SUB] on antiviral signalling in the respiratory epithelium using the bronchial Calu-3 cell line grown at the air-liquid interface. Pre-exposure to PM[SUB]2.5[/SUB] 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 PM[SUB]2.5[/SUB] on viral replication was observed during co-exposure, although a downregulation of IFN-β release was associated to PM[SUB]2.5[/SUB] 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 PM[SUB]2.5[/SUB] could alter the antiviral response of bronchial epithelial cells, increasing their susceptibility to viral infection.
Keywords: Antiviral signalling pathways; Co-exposure; Inflammation; Interferon; PM(2.5)/virus interaction; Pre-exposure.
. 2024 Mar 14:123781.
doi: 10.1016/j.envpol.2024.123781. Online ahead of print. Exposure to PM[SUB]2.5[/SUB] modulate the pro-inflammatory and interferon responses against influenza virus infection in a human 3D bronchial epithelium model
Chloé Chivé[SUP] 1 [/SUP], Lydie Martίn-Faivre[SUP] 2 [/SUP], Alice Eon-Bertho[SUP] 3 [/SUP], Christelle Alwardini[SUP] 3 [/SUP], Jéril Degrouard[SUP] 4 [/SUP], Alexandre Albinet[SUP] 5 [/SUP], Gael Noyalet[SUP] 6 [/SUP], Servanne Chevaillier[SUP] 6 [/SUP], Franck Maisonneuve[SUP] 7 [/SUP], Jean-Michel Sallenave[SUP] 2 [/SUP], Stéphanie Devineau[SUP] 3 [/SUP], Vincent Michoud[SUP] 6 [/SUP], Ignacio Garcia-Verdugo[SUP] 8 [/SUP], Armelle Baeza-Squiban[SUP] 3 [/SUP]
Affiliations
- PMID: 38492752
- DOI: 10.1016/j.envpol.2024.123781
Epidemiological studies showed a positive association between exposure to PM[SUB]2.5[/SUB] and the severity of influenza virus infection. However, the mechanisms by which PM[SUB]2.5[/SUB] can disrupt antiviral defence are still unclear. From this perspective, the objective of this study was to evaluate the effects of PM[SUB]2.5[/SUB] on antiviral signalling in the respiratory epithelium using the bronchial Calu-3 cell line grown at the air-liquid interface. Pre-exposure to PM[SUB]2.5[/SUB] 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 PM[SUB]2.5[/SUB] on viral replication was observed during co-exposure, although a downregulation of IFN-β release was associated to PM[SUB]2.5[/SUB] 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 PM[SUB]2.5[/SUB] could alter the antiviral response of bronchial epithelial cells, increasing their susceptibility to viral infection.
Keywords: Antiviral signalling pathways; Co-exposure; Inflammation; Interferon; PM(2.5)/virus interaction; Pre-exposure.