Colonization, mortality, and host cytokines response to enterohemorrhagic Escherichia coli in rabbits

The major virulence factor of enterohemorrhagic Escherichia coli in infections is its ability to cause attaching and effacing lesions in enterocytes, as well as to produce Shiga toxins. To clarify the pathogenic mechanism and host innate immune responses of enterohemorrhagic Escherichia coli in rabbits, experimental infections with TS and MY strains were conducted. Among the results, although the MY strain's pathogenicity was stronger than the TS, typical symptoms were observed in both groups of bacterial-infected rabbits. Pathological changes in the heart, liver, and spleen of rabbits infected with the MY strain were more severe than those infected with the TS strain, pro-inflammatory cytokines IL-1β, IL-6, IL-8, IFN-γ, and TNF-α were induced by both strains, and α- and β-defensin were significantly upregulated at 3 d postinfection. Moreover, in the spleen, the MY strain induced greater expressions of α- and β-defensins than did the TS strain. However, in the liver, the TS strain induced greater expressions of α- and β-defensins than did the MY strain. Most likely, different replications of the MY and TS strains in the liver and spleen induced different host immune responses. Altogether, the findings provide new insights into the occurrence and development of enterohemorrhagic Escherichia coli-mediated diseases in rabbits.