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

Wenhao Yang,Tongjie Chai,Liangmeng Wei,Xinyu Wang,Fahao Wu,Guangen Hao,Mengjiao Guo,Rong Li

doi:10.18632/oncotarget.20966

Abstract

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.

Highlights

Enterohemorrhagic Escherichia coli (EHEC) belongs to the family of Shiga toxins (Stxs)-producing E. coli, many of whose members carry the eae gene and can cause severe disease [1]
Pathological changes in rabbits infected with the MY strain were more serious than those infected with the TS strain
Used as a food source, as experimental animals, and as household pets, rabbits suffer from diarrhea and even rapid death due to EHEC infection during breeding

Summary

Introduction

Enterohemorrhagic Escherichia coli (EHEC) belongs to the family of Shiga toxins (Stxs)-producing E. coli, many of whose members carry the eae gene and can cause severe disease [1]. As A-B-type toxins, Stxs are considered to be major virulence factors in the pathogenesis of haemolytic uremic syndrome and hemorrhagic colitis [2]. Enterohemorrhagic Escherichia coli (EHEC) was first isolated in 1977 by Konowalchuk et al [4]. In 1982, the bacterium first caused an outbreak of hemorrhagic enteritis in North America and was named EHEC [5]. In Japan, the EHEC infection broke out in 1996. In United States, an outbreak of EHEC infection occurred in 2006. The outbreak of EHEC in developed countries such as the United States, Japan, Canada and the United Kingdom showed a trend of increasing year by year

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