Research Papers: Immunology:
Colonization, mortality, and host cytokines response to enterohemorrhagic Escherichia coli in rabbits
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Mengjiao Guo1,2, Wenhao Yang1, Fahao Wu1, Guangen Hao1, Rong Li1, Xinyu Wang1, Liangmeng Wei1,2 and Tongjie Chai1
1 College of Animal Science and Veterinary Medicine, Sino-German Cooperative Research Centre for Zoonosis of Animal Origin of Shandong Province, Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, Tai’an, Shandong, China
2 Collaborative Innovation Center for the Origin and Control of Emerging Infectious Diseases, Taishan Medical University, Taian City, China
Liangmeng Wei, email:
Tongjie Chai, email:
Keywords: enterohemorrhagic Escherichia coli, pathogenicity, innate immunity, cytokines, rabbits, Immunology and Microbiology Section, Immune response, Immunity
Received: July 26, 2017 Accepted: September 03, 2017 Published: September 16, 2017
The major virulence factor of enterohemorrhagic Escherichia coli in infections is its ability to cause attaching and effacinglesions 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 theTS 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.
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