Acid and Bile-Salt Stress of Enteropathogenic Escherichia coli Enhances Adhesion to Epithelial Cells and Alters Glycolipid Receptor Binding Specificity

• Published in: The Journal of infectious diseases 2005-10, Vol.192 (8), p.1430-1440
• Main Authors: de Jesus, Margaret C., Urban, Agnieszka A., Marasigan, Marastella E., Barnett Foster, Debora E.
• Format: Article
• Language: English
• Subjects: Acids - pharmacology; Adhesins, Escherichia coli - metabolism; Bacteria; Bacterial adhesion; Bacterial Adhesion - drug effects; Bacterial Adhesion - physiology; Bacteriology; Bile acids; Bile Acids and Salts - pharmacology; Biological and medical sciences; Cell adhesion; Cell Culture Techniques; Epithelial cells; Epithelial Cells - metabolism; Escherichia coli; Escherichia coli - drug effects; Escherichia coli - metabolism; Escherichia coli - pathogenicity; Flagella; Fundamental and applied biological sciences. Psychology; HSP70 Heat-Shock Proteins; Humans; Infectious diseases; Intestinal Mucosa - immunology; Intestinal Mucosa - microbiology; Medical sciences; Microbiology; Miscellaneous; Receptors; Receptors, Cell Surface - metabolism; Viability
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/462422

Background Enteropathogenic Escherichia coli (EPEC), a diarrheagenic pathogen, is exposed to stress during ingestion, and yet little is known about the impact of stress on EPEC–host cell adhesion MethodsEPEC adhesion to human epithelial cells was assessed by plate-count assay before and after bacterial stress. Stress treatments included exposure to low pH (with or without acid adaptation) and exposure to physiological concentrations of 4 intestinal bile salts. Expression of bacterial adhesins after stress was assessed by immunoblot and flow-cytometric analysis. Bacteria-lipid binding was determined by thin-layer chromatography overlay assay ResultsBrief low-pH stress (with or without acid adaptation) and bile-salt stress resulted in significantly increased EPEC–host cell adhesion. Erythromycin pretreatment eliminated the adhesion enhancement, suggesting that protein synthesis was required. Immunoblot and flow-cytometric analysis indicated little change in expression of known adhesins after either stress. However, we found increased surface expression of a heat-shock protein 70 (Hsp70) on acid-shocked EPEC, and pretreatment with anti-Hsp70 eliminated the adhesion enhancement after acid stress. Acid shock also correlated with increased binding to sulfogalactosylceramide, a putative receptor for other pathogens after stress ConclusionsAcid/bile-salt stress of EPEC significantly enhances adhesion to host cells, and a novel adhesin-receptor pair may play a role in the adhesion