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  • Title: Differential gene expression profiling of porcine epithelial cells infected with three enterotoxigenic Escherichia coli strains.
    Author: Zhou C, Liu Z, Jiang J, Yu Y, Zhang Q.
    Journal: BMC Genomics; 2012 Jul 23; 13():330. PubMed ID: 22823589.
    Abstract:
    BACKGROUND: Enterotoxigenic Escherichia coli (ETEC) is one of the most important pathogenic bacteria causing severe diarrhoea in human and pigs. In ETEC strains, the fimbrial types F4 and F18 are commonly found differently colonized within the small intestine and cause huge economic losses in the swine industry annually worldwide. To address the underlying mechanism, we performed a transcriptome study of porcine intestinal epithelial cells (IPEC-J2) with and without infection of three representative ETEC strains. RESULTS: A total 2443, 3493 and 867 differentially expressed genes were found in IPEC-J2 cells infected with F4ab ETEC (C(F4ab)), with F4ac ETEC (C(F4ac)) and with F18ac ETEC (C(F18ac)) compared to the cells without infection (control), respectively. The number of differentially expressed genes between C(F4ab) and C(F4ac), C(F4ab) and C(F18ac), and C(F4ac) and C(F18ac) were 77, 1446 and 1629, respectively. The gene ontology and pathway analysis showed that the differentially expressed genes in C(F4ab)vs control are significantly involved in cell-cycle progress and amino acid metabolism, while the clustered terms of the differentially expressed genes in C(F4ac)vs control comprise immune, inflammation and wounding response and apoptosis as well as cell cycle progress and proteolysis. Differentially expressed genes between C(F18ac)vs control are mainly involved in cell-cycle progression and immune response. Furthermore, fundamental differences were observed in expression levels of immune-related genes among the three ETEC treatments, especially for the important pro-inflammatory molecules, including IL-6, IL-8, TNF-α, CCL20, CXCL2 etc. CONCLUSIONS: The discovery in this study provides insights into the interaction of porcine intestinal epithelial cells with F4 ETECs and F18 ETEC, respectively. The genes induced by ETECs with F4 versus F18 fimbriae suggest why ETEC with F4 may be more virulent compared to F18 which seems to elicit milder effects.
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