Chronic alcohol consumption dysregulates innate immune response to SARS-CoV-2 in the lung.
Sloan A LewisIsaac R CincoBrianna M DorattMadison B BlantonCherise HoaglandMichael DaviesKathleen A GrantIlhem MessaoudiPublished in: bioRxiv : the preprint server for biology (2023)
Alcohol consumption is widespread with over half of the individuals over 18 years of age in the U.S. reporting alcohol use in the last 30 days. Moreover, 9 million Americans engaged in binge or chronic heavy drinking (CHD) in 2019. CHD negatively impacts pathogen clearance and tissue repair, including in the respiratory tract, thereby increasing susceptibility to infection. Although, it has been hypothesized that chronic alcohol consumption negatively impacts COVID-19 outcomes; the interplay between chronic alcohol use and SARS-CoV-2 infection outcomes has yet to be elucidated. Therefore, in this study we investigated the impact of chronic alcohol consumption on SARS-CoV-2 anti-viral responses in bronchoalveolar lavage cell samples from humans with alcohol use disorder and rhesus macaques that engaged in chronic drinking. Our data show that in both humans and macaques, the induction of key antiviral cytokines and growth factors was decreased with chronic ethanol consumption. Moreover, in macaques fewer differentially expressed genes mapped to Gene Ontology terms associated with antiviral immunity following 6 month of ethanol consumption while TLR signaling pathways were upregulated. These data are indicative of aberrant inflammation and reduced antiviral responses in the lung with chronic alcohol drinking.
Keyphrases
- alcohol consumption
- sars cov
- emergency department
- drug induced
- stem cells
- respiratory tract
- genome wide
- bone marrow
- signaling pathway
- skeletal muscle
- metabolic syndrome
- big data
- innate immune
- machine learning
- electronic health record
- coronavirus disease
- cell proliferation
- respiratory syndrome coronavirus
- transcription factor
- inflammatory response
- single cell
- nuclear factor
- weight loss
- data analysis
- endoplasmic reticulum stress
- adverse drug