SteE促进鸡体内白痢沙门氏菌的定植

Zhike Liu, A. Fotin, R. Petrov, Jinyou Ma, T. Fotina
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摘要

白痢沙门氏菌(S. pullorum)是白痢病的病原体,对家禽造成严重的经济损失,并能通过定殖宿主器官长期存活。steE是沙门氏菌致病性岛2分泌的效应蛋白。沙门氏菌在体内的定植尚不清楚。为了研究steE对鸡白痢沙门氏菌在鸡主要器官中的定殖作用,我们分别用鸡白痢沙门氏菌和鸡白痢沙门氏菌ΔsteE株免疫鸡。毒力测定结果表明,鸡体内白痢沙门氏菌ΔsteE的LD50是白痢沙门氏菌的22.8倍。细菌定殖实验表明,鸡肝脏、脾脏、心脏、滑囊和盲肠中白痢沙门氏菌和白痢沙门氏菌ΔsteE菌株数量的总体变化趋势相似,均呈现先增加后减少的趋势。然而,在鸡感染模型中,steE的缺失导致鸡白痢沙门氏菌的定植、病理改变和毒力显著降低。我们的研究结果提供了令人兴奋的见解致病机制和减毒活疫苗与猪链球菌e相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
SteE enhances the colonization of Salmonella Pullorum in chickens
Salmonella pullorum (S. pullorum) is the causative agent of pullorum disease and results in severe economic losses in poultry, and can long-term survival by colonizing host organs. steE is an effector protein secreted by Salmonella pathogenicity island 2. It is not clear in vivo for the colonization of Salmonella. To investigate the role of steE on the colonization of S. Pullorum in the principal organs of chicken, we used S. pullorum and S. pullorum ΔsteE strains immunized chickens, respectively. The results of the virulence assay showed that the LD50 of S. pullorum ΔsteE was 22.8 times higher than that of S. pullorum in chickens. The colonization experiment of bacteria showed that the overall change trend of the number of S. pullorum and S. pullorum ΔsteE strains were similar in chicken liver, spleen, heart, bursa, and cecum, which increased first and then decreased. However, the deletion of steE caused significantly reduced colonization, pathological change, and virulence of S. pullorum in a chicken infection model. Our findings provide exciting insights into the pathogenic mechanism and live attenuated vaccine associated with steE in S. pullorum.
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