Lactobacillus amylophilus D14 protects tight junction from enteropathogenic bacteria damage in Caco-2 cells

Abstract

Enterotoxigenic Escherichia coli and Salmonella Typhimurium could adhere to epithelial tissue and destroy cell junctions, leading to intestinal inflammation and diarrhea. Lactobacillus could prevent the adhesion of pathogens to host cells and protect the mucosal barrier. The objective of this study was to investigate the protective effects of Lactobacillus amylophilus D14 on Caco-2 cells against the invasion of enterotoxigenic Escherichia coli K88 and Salmonella Typhimurium SL1344. We found that with a reduction in dextran permeability and an increase in transepithelial electrical resistance, L. amylophilus D14 could ameliorate the damage to cell integrity caused by pathogens. Furthermore, L. amylophilus D14 reduced the expression of phosphorylated extracellular signal-regulated protein kinase and phospho-c-jun N-terminal kinase, and it decreased the secretion of IL-8. The abilities of the Lactobacillus to protect the cell junctions were then evaluated on Caco-2 cells. Increased expression and amelioration distribution of tight junction proteins (zonula occludens-1, claudin-1, and E-cadherin) were observed when the cells were cocultured with pathogens and Lactobacillus simultaneously. Lactobacillus amylophilus D14 may influence the mitogen-activated protein kinase pathway to regulate the correct assembly of the tight junction and adherens junction, protecting the cell junctions and mucosal barrier damaged by enterotoxigenic E. coli K88 or Salmonella Typhimurium SL1344 infection.