Summary auto-generated
This research article investigates the adhesion and invasion of pathogenic Escherichia coli and Salmonella strains to intestinal epithelial cells and mucus. The study examined several bacterial strains including enterohemorrhagic E. coli O157:H7, enteropatogenic E. coli O111, nonpathogenic E. coli K12, and Salmonella enterica serovar Typhimurium (Stm). Researchers tested bacterial interactions with cultured intestinal cell lines and explored the roles of specific bacterial surface structures and adhesins in pathogenic colonization. The experiments involved exposing bacterial cultures to epithelial cells under various conditions and measuring bacterial attachment, invasion rates, and cellular responses. Key virulence factors including flagella, type III secretion systems, and outer membrane proteins were examined. The results demonstrated differential adherence patterns among the bacterial strains, with pathogenic strains showing enhanced ability to attach to and invade intestinal epithelial cells compared to nonpathogenic K12. The study contributes to understanding molecular mechanisms of bacterial pathogenesis and identifies potential targets for intervention against enteric infections caused by these clinically important gram-negative pathogens.
Key findings
- Pathogenic E. coli O157:H7 and O111 strains demonstrated significantly higher adhesion and invasion rates to intestinal epithelial cells compared to nonpathogenic K12 strain
- Type III secretion systems and flagellar structures played important roles in bacterial attachment and epithelial cell invasion
- Salmonella enterica Typhimurium showed distinct adhesion patterns compared to E. coli strains, with differential reliance on specific virulence factors
- Mucus layer interactions varied among bacterial strains, affecting their ability to reach and colonize epithelial cells
- Specific bacterial outer membrane proteins and adhesins were identified as critical determinants of pathogenic colonization efficiency
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Abstract
Sections of kidney, trachea, ileum, colon, rectum and rumen were removed at post mortem from a neonatal calf and, with the exception of the rumen, primary cell lines were established for each of the cell types. The adherence of enterohaemorrhagic Escherichia coli (EHEC) serotype O157:H7, enteropathogenic E. coli (EPEC) serotype O111, E. coli K12 (a laboratory adapted non-pathogenic strain) and Salmonella enterica serotype Typhimurium was assayed on each cell type. For all adherence assays on all cell lines, EHEC O157:H7 adhered to a significantly greater extent than the other bacteria. S. Typhimurium and EPEC O111 adhered to a similar extent to one another, whereas E. coli K12 was significantly less adherent by 100-fold. In all cell types, >10% of adherent S. Typhimurium bacteria invaded, whereas c. 0.010.1% of adherent EHEC O157:H7 and EPEC O111 bacteria invaded, although they are regarded as non-invasive. EHEC O157 generated actin re-arrangements in all cell types as demonstrated by fluorescent actin staining (FAS) under densely packed bacterial micro-colonies. EPEC O111 readily generated the localised adherent phenotype on bovine cells but generated only densely packed micro-colonies on HEp-2 cells. The intensity of actin re-arrangements induced in bovine cells by EPEC O111 was less than that induced by EHEC O157:H7. The intimate attachment on all cell types by both EHEC O157:H7 and EPEC O111 was clearly demonstrated by scanning electron microscopy.