Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10137369 | Research in Veterinary Science | 2018 | 6 Pages |
Abstract
To investigate the effects of pathogenic Escherichia coli high pathogenicity island (HPI) on the expression of inflammatory factors via ubiquitin proteasome pathway. Firstly, the UBC-sus-263 shRNA plasmid was successfully established and transfected into porcine small intestine epithelial cells (IPEC-J2) by liposome to silence the ubiquitinntion gene. Then the IPEC-J2 was infected with E. coli HPI+ and HPIâ strains, respectively. Finally, the mRNA of intracellular NF-κB and IκB-α,and the protein levels of NF-κB, IκB-α, TNF-α and IL-1 in IPEC-J2 cell line transfected with UBC-sus-263 shRNA (Ub-shRNA) were detected. The results showed that the Ub-shRNA was effectively inhibited ubiquitination pathway in the IPEC-J2 cell. After infected with HPI+, the mRNA and protein levels of NF-κB and IκB-α were dramatically decreased in Ub-hsRNA transfected IPEC-J2 cells compared to the control and HPIâ-infected groups. Consistently, the production of downstream cytokines such as TNF-α and IL-1 were highly expressed after HPI+-infection than that of HPIâ-infected groups. However, whether the HPI+ or HPIâ, both could induce increasingly expression of NF-κB and IκB-α and its downstream cytokines in normal IPEC-J2 cells. Thus, the E. coli HPI can upregulate the expression of IκB-α to promote the releasing of TNF-α and IL-1 via the ubiquitination pathway.
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Authors
Chaoying Liu, Chunlan Shan, Qin Dong, Guowen Fu, Ru Zhao, Yulin Yan, Hong Gao,