Respiratory Syncytial Virus-Induced Host IFN Signaling Differs Between A549 and BEAS-2B Epithelial Cell Lines

Hillyer, Philippa; Shepard, Rachel; Uehling, Megan; Sheik, Faruk; Luongo, Cindy; Buchholz, Ursula J.; Collins, Peter L.; Donnelly, Raymond P.; Rabin, Ronald L.

doi:10.1016/j.jaci.2014.12.964

Cited by 2 publications

(1 citation statement)

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“…With regard to immunological factors, we found that RSV infection induces robust secretion of both cytokines (particularly, IFN-L1 and TNF-α) and chemokine (particularly, IP10/CXCL10). RSV-induced higher IFN-L1 level was also observed in previous studies [76, 77]. We also found a substantial induction of proinflammatory cytokine TNF-α, which is part of the NF-kB signaling pathway and is considered the central activator of inflammation and innate immunity in response to RSV infection [57, 78, 79].…”

Section: Discussionsupporting

confidence: 88%

RSV-induced Expanded Ciliated Cells Contribute to Bronchial Wall Thickening

Talukdar¹,

Osan²,

Ryan³

et al. 2022

Preprint

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Viral infection, particularly respiratory syncytial virus (RSV), causes inflammation in the bronchiolar airways (bronchial wall thickening, also known as bronchiolitis), reducing airflow through the bronchioles. This bronchial wall thickening is a common pathophysiological feature in RSV infection, but it causes more fatalities in infants than in children and adults. However, the molecular mechanism of RSV-induced bronchial wall thickening remains unknown, particularly in healthy adults. RSV infection in the airway epithelium of healthy adult bronchial cells reveals RSV-infects primarily ciliated cells. RSV infection expands the cell cytoskeleton substantially without compromising epithelial membrane integrity and ciliary functions. The RSV-induced actin cytoskeleton expansion increases ununiformly epithelial height, and cytoskeletal (actin polymerization), immunological (INF-L1, TNF-α, IP10/CXCL10), and viral (NS2) factors are probably responsible. Interestingly, RSV-infected cell cytoskeleton’s expansion resembles a noncanonical inflammatory phenotype, which contributes to bronchial wall thickening, and is termed cytoskeletal inflammation.

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