Alcohol‐induced altered glycans in human tracheal epithelial cells promote bacterial adhesion
Heavy alcohol drinking is known to increase the risk of bacterial pneumonia. However, the link between alcohol levels and risk of infection remains underexplored. Recently, we found that alcohol induced α2-6sialo mucin O-glycans in human tracheobronchial epithelial cells, which mediated the killing of U937 macrophages. By extending this study, we focus here on whether altered glycans induced by alcohol in human airway epithelial cells can promote adhesion of Klebsiella pneumoniae (Kp) and Streptococcus pneumoniae (Sp). We have found that exposure of human tracheal epithelial cells to alcohol also induces high mannose N-glycans terminated with α3mannose and increases adhesion of Kp, which is inhibited by αmethylmannoside or aldehyde dehydrogenase 2 activator 1. Further, the α2-6sialo mucin O-glycans induced by alcohol in human tracheal epithelial cells also enhance the adhesion of Sp, which is inhibited by ovine submaxillary mucin or aldehyde dehydrogenase 2 activator 1. We conclude that alcohol induces altered glycans in human airway epithelial cells, which increase the risk of bacterial pneumonia by compromising immune function and promoting the adhesion of Kp and Sp.
Authors
- Souvik Datta (ORCID: https://orcid.org/0000-0001-8274-2435)
- Derrick R. Samuelson (ORCID: https://orcid.org/0000-0002-5356-1413)
- Pi‐Wan Cheng
Institutions
- University of Nebraska Medical Center (US)
Publication Details
- Journal
- FEBS Open Bio
- Published
- 2025-12-21
- DOI
- https://doi.org/10.1002/2211-5463.70188
- Primary Topic
- Alcohol Consumption and Health Effects
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- U.S. Department of Health and Human Services
- University of Nebraska Medical Center
- Nebraska Department of Health and Human Services
- National Institutes of Health