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Respiratory viruses and the inflammasome: The double-edged sword of inflammation
Journal article   Open access   Peer reviewed

Respiratory viruses and the inflammasome: The double-edged sword of inflammation

Kody A Waldstein and Steven M Varga
PLoS pathogens, Vol.18(12), p.e1011014
12/2022
DOI: 10.1371/journal.ppat.1011014
PMCID: PMC9799286
PMID: 36580480
url
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9799286/View
Published (Version of record) Open Access

Abstract

Individuals actively infected with respiratory viruses, such as influenza A virus (IAV), respiratory syncytial virus (RSV), and coronaviruses, transmit by shedding droplets containing live virus while coughing, sneezing, or talking. Respiratory viruses subsequently enter the airways of a host either by coming in direct contact with aerosolized droplets or by an interaction with fomites. The majority of respiratory virus infections are contained to the upper airways and self-limiting; however, lower respiratory tract infections (LRTIs) are a significant cause of morbidity and mortality, especially in children and the elderly. When infiltration into the lower airways occurs, infectious viral particles encounter lung resident alveolar macrophages (AMϕ). AMϕ are self-renewing fetal-derived sentinel cells present in the airways that are tethered to the lung epithelium through αvβ6 integrin-latent TGF-β binding. Upon direct interaction with viral particles, pro-inflammatory cytokines, or pattern/danger-associated molecular patterns (PAMPs/DAMPs), AMϕ detach from the respiratory epithelium resulting in the induction of increased effector functions and phagocytosis as well as the up-regulation of type I interferons (IFN), chemokines, and pro-inflammatory cytokines.
Inflammation Humans Inflammasomes Viruses RSV IAV coronavirus

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