Effect of high-pathogenicity island (HPI) on TGF-β1/Smad3 pathway in mouse model of E. coli strains causing diarrhea in calf

Abstract

PurposeThis study evaluated pathogenic effect of TGF-β1/Smad3 pathway in mouse model after infecting them with HPI+ and HPI− strains of Escherichia coli (E. coli) which were isolated from diarrhea in calves. MethodsKunming mice were randomly divided into 3 groups: a control group, HPI+-infection group and HPI−-infection group. After intraperitoneal injection of HPI strains of E. coli (concentration: 3 × 108 cfu/mL) in mice, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) contents were detected at 12 h post infection. The sections of liver and kidney were obtained for histopathological observations. Propidium iodide and 4′,6-diamidino-2-phenylindole (DAPI) staining was used to analyze the cell apoptosis. The immunohistochemistry staining and quantitative real time PCR (q-PCR) were performed for evaluating the protein and mRNA expression of TGF-β1, Collagen I and Smad3. The histological change and PI staining of liver and kidney showed significant injuries. Compared with the control group, the serum ALT and AST activities and TNF-α and IL-6 contents of mice in the HPI+ and HPI− groups were increased, number of apoptotic cells and expression of TGF-β1, Collagen Iand Smad3 were up-regulated after E. coli infection in liver and kidney, which was significantly increased in HPI+-infected compared to HPI−. ConclusionThe study concludes that E. coli HPI induced and enhanced the over expression of TGF-β1/Smad3 pathway and ultimately caused pathological anomalies.