Injury and mechanism of recombinant <i>E. coli</i> expressing STa on piglets colon

Abstract

Enterotoxigenic Escherichia coli (ETEC) is primary pathogenic bacteria of piglet diarrhea, over two thirds of piglets diarrhea caused by ETEC are resulted from STa-producing ETEC strains. This experiment was conducted to construct the recombinant E. coli expressing STa and study the injury and mechanism of recombinant E. coli expressing STa on 7 days old piglets colon. Twenty-four 7 days old piglets were allotted to four treatments: control group, STa group (2 × 109 CFU E. coli LMG194-STa), LMG194 group (2 × 109 CFU E. coli LMG194) and K88 group (2 × 109 CFU E. coli K88). The result showed that E. coli infection significantly increased diarrhea rates; changed DAO activity in plasma and colon; damaged colonic mucosal morphology including crypt depth, number of globet cells, density of lymphocytes and lamina propria cell density; substantially reduced antioxidant capacity by altering activities of GSH-Px, SOD, and TNOS and productions of MDA and H2O2; obviously decreased AQP3, AQP4 and KCNJ13 protein expression levels; substantially altered the gene expression levels of inflammatory cytokines. Conclusively, STa group had the biggest effect on these indices in four treatment groups. These results suggested that the recombinant strain expressed STa can induce piglets diarrhea and colonic morphological and funtional damage by altering expression of proteins connect to transportation function and genes associated with intestinal injury and inflammatory cytokines.

Regulatory Effect of Methylation of the Porcine AQP3 Gene Promoter Region on Its Expression Level and Porcine Epidemic Diarrhea Virus Resistance

“…Subsequent qPCR analysis revealed that AQP3 expression in the small intestine of PEDV-infected piglets was extremely significantly downregulated compared with normal piglets, with the most significant decrease in the jejunum tissue. Lv et al reported the same trend of AQP3 expression in the colon of pigs with diarrhea caused by enterotoxigenic E. coli (ETEC) [ 28 ]. Studies have shown that AQP3 expression is competitively regulated by miR-874 and lncRNA H19, which in turn opens the tight junction complex, resulting in decreased occludin and claudin-1 protein expression and increased intestinal permeability [ 29 , 30 ].…”

Enterotoxigenic Escherichia coli Heat-Stable Toxin Increases the Rate of Zinc Release from Metallothionein and Is a Zinc- and Iron-Binding Peptide

“…Moreover, lactoferrin inhibited adherence of ETEC to both human epithelial cells and to the intestinal mucosa of germfree mice (68). Host metal-binding proteins calprotectin, myeloperoxidase, and lactoferrin, typically derived from host neutrophils, have become fecal markers of ETEC infection, and recent studies have shown that these biomarkers can be used to assess the burden of enteric infections (42,65,(69)(70)(71).…”

Events associated with susceptibility to invasive Salmonella enterica serovar Typhi in BALB/c mice previously infected with Plasmodium berghei ANKA

“…Changes in the architecture of the intestinal tissue included the increase in the number of goblet cells and in the cell density, which in the latter is characterized by volume of the leukocyte infiltrate in the sub-mucosa. The goblet cells are responsible for the layer of mucus that covers the epithelium to facilitate the removal of food content and are also part of the first line of defense against damage caused by pathogenic bacteria and bacterial products 27 , 28 . Here, coinfected mice showed several of these mucoid cells in the enterocyte layer, which indicates that the innate response to the infection bacteria was active in these animals.…”