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SteE通过调节炎症反应增强鸡白痢杆菌在鸡体内的毒力。

SteE Enhances the Virulence of Pullorum in Chickens by Regulating the Inflammation Response.

作者信息

Liu Zhike, Wang Li, Yu Yan, Fotin Anatoliy, Wang Qiuxia, Gao Pei, Zhang Yanhong, Fotina Tetiana, Ma Jinyou

机构信息

College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang, China.

Faculty of Veterinary Medicine, Sumy National Agrarian University, Sumy, Ukraine.

出版信息

Front Vet Sci. 2022 Jul 14;9:926505. doi: 10.3389/fvets.2022.926505. eCollection 2022.

DOI:10.3389/fvets.2022.926505
PMID:35909683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9330158/
Abstract

serovar Pullorum (. Pullorum) is a host-specific pathogen, which causes acute gastroenteritis with high mortality in poultry. However, the association between , encoded by type III secretion system 2, and virulence is not well-understood. To elucidate the functions of in . Pullorum, Δ strain was constructed using the λ-Red recombination technology. Compared to that in the wild-type, the deletion of in . Pullorum reduced bacterial invasion, proliferation, and late apoptosis in the infected HD-11 cells. In addition, we analyzed the mRNA expression levels of effector genes and cytokines by qRT-PCR. was associated with the regulation of various effector genes and inflammatory cytokines in HD-11 cells during . Pullorum infection. The wild-type effector promoted the expression of anti-inflammatory cytokines (IL-4 and IL-10) and reduced that of pro-inflammatory cytokines (IL-1β, IL-6, and IL-12) compared to that in the Δ-infected HD-11 cells and chicken spleens. Results from the chicken infection model showed that the deletion of resulted in significantly decreased colonization and long-term survival of the bacteria and alleviated pathological lesions compared to those in the wild-type. Further, increased the virulence of . Pullorum in chickens by regulating the expression of inflammatory cytokines. Our findings provide insights into the persistent infection and autoimmunity associated with in . Pullorum.

摘要

鸡白痢沙门氏菌（鸡白痢杆菌）是一种宿主特异性病原体，可导致家禽急性肠胃炎并伴有高死亡率。然而，由III型分泌系统2编码的[具体基因名称未给出]与鸡白痢杆菌毒力之间的关联尚未得到充分理解。为阐明[具体基因名称未给出]在鸡白痢杆菌中的功能，利用λ-Red重组技术构建了缺失该基因的菌株。与野生型相比，鸡白痢杆菌中该基因的缺失降低了其在感染的HD-11细胞中的细菌侵袭、增殖及晚期凋亡。此外，我们通过qRT-PCR分析了效应基因和细胞因子的mRNA表达水平。在鸡白痢杆菌感染期间，[具体基因名称未给出]与HD-11细胞中各种效应基因和炎性细胞因子的调控相关。与感染缺失该基因菌株的HD-11细胞和鸡脾脏相比，野生型效应蛋白[具体名称未明确]促进了抗炎细胞因子（IL-4和IL-10）的表达，并降低了促炎细胞因子（IL-1β、IL-6和IL-12）的表达。鸡感染模型的结果表明，与野生型相比，该基因的缺失导致细菌的定殖和长期存活显著降低，并减轻了病理损伤。此外，[具体基因名称未给出]通过调节炎性细胞因子的表达增加了鸡白痢杆菌在鸡体内的毒力。我们的研究结果为鸡白痢杆菌中与[具体基因名称未给出]相关的持续感染和自身免疫提供了见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c158/9330158/94138d56a797/fvets-09-926505-g0007.jpg
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