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鸡伤寒沙门氏菌基因在鸡伤寒的全身感染中起关键作用。

Gene of Gallinarum Plays a Critical Role in Systemic Infection of Fowl Typhoid.

作者信息

Ojima Shinjiro, Ono Hisaya K, Okimoto Ryo, Yu Xiaoying, Sugiyama Makoto, Yoshioka Kazuki, Haneda Takeshi, Okamura Masashi, Hu Dong-Liang

机构信息

Laboratory of Zoonoses, Kitasato University School of Veterinary Medicine, Towada, Japan.

College of Animal Science, Jilin Agricultural University, Changchun, China.

出版信息

Front Microbiol. 2022 May 26;13:880932. doi: 10.3389/fmicb.2022.880932. eCollection 2022.

DOI:10.3389/fmicb.2022.880932
PMID:35694286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9178343/
Abstract

serovar Gallinarum (. Gallinarum) is a host-specific pathogen causing fowl typhoid, a severe systemic infection in poultry, which leads to substantial economic losses due to high morbidity and mortality in many developing countries. However, less is known about the pathogenic characteristics and mechanism of . Gallinarum-induced systemic infection in chickens. In this study, we deleted the . Gallinarum UDP--acetylglucosamine-1-phosphate transferase gene, which contributes to the biosynthesis of enterobacterial common antigen (ECA), and studied the pathogenicity of this ::Cm strain in a chicken model of systemic infection. The ::Cm mutant strain showed comparable growth but lower resistance to bile acid and nalidixic acid than the wild-type strain . In the oral infection model of chickens, the virulence of the ::Cm strain was significantly attenuated . Chickens infected with wild-type strain showed typical clinical signs and pathological changes of fowl typhoid and died between 6 and 9 days post-infection, and the bacteria rapidly disseminated to systemic organs and increased in the livers and spleens. In contrast, the ::Cm mutant strain did not cause chicken death, there were no significant clinical changes, and the bacterial numbers in the liver and spleen of the chickens were significantly lower than those of the chickens infected with the wild-type strain. In addition, the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and CXCLi1 in the livers of ::Cm-infected chickens was significantly lower than that of the chickens infected with the wild-type strain. Furthermore, the attenuated ::Cm strain could persistently colonize the liver and spleen at low levels for up to 25 days post-infection and could induce a protective immune response in the chickens. These results indicate that the gene is an important virulence factor of . Gallinarum in the chicken model of systemic infection, and the avirulent ::Cm mutant could possibly be used as a live-attenuated vaccine strain for controlling fowl typhoid.

摘要

鸡伤寒沙门氏菌血清型鸡伤寒亚种(. Gallinarum)是一种宿主特异性病原体,可引起禽伤寒,这是一种在家禽中发生的严重全身性感染,在许多发展中国家,由于其高发病率和死亡率导致了巨大的经济损失。然而,关于. Gallinarum诱导鸡全身性感染的致病特征和机制知之甚少。在本研究中,我们删除了. Gallinarum的UDP - N - 乙酰葡糖胺 - 1 - 磷酸转移酶基因,该基因有助于肠道细菌共同抗原(ECA)的生物合成,并在全身性感染的鸡模型中研究了该 ::Cm菌株的致病性。与野生型菌株相比, ::Cm突变株显示出相当的生长能力,但对胆汁酸和萘啶酸的抵抗力较低。在鸡的口服感染模型中, ::Cm菌株的毒力显著减弱。感染野生型菌株的鸡表现出禽伤寒的典型临床症状和病理变化,并在感染后6至9天死亡,细菌迅速扩散到全身器官,并在肝脏和脾脏中增加。相比之下, ::Cm突变株未导致鸡死亡,没有明显的临床变化,并且鸡肝脏和脾脏中的细菌数量显著低于感染野生型菌株的鸡。此外,感染 ::Cm的鸡肝脏中白细胞介素(IL)-1β、肿瘤坏死因子(TNF)-α和CXCLi1的表达明显低于感染野生型菌株的鸡。此外,减毒的 ::Cm菌株在感染后长达25天可在肝脏和脾脏中低水平持续定殖,并可在鸡中诱导保护性免疫反应。这些结果表明,该基因是. Gallinarum在全身性感染鸡模型中的重要毒力因子,无毒的 ::Cm突变株可能用作控制禽伤寒的减毒活疫苗株。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/f704a23ead58/fmicb-13-880932-g0007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/f8214abdc4af/fmicb-13-880932-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/f704a23ead58/fmicb-13-880932-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/ee79c2ad414c/fmicb-13-880932-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/a945b8dc0f84/fmicb-13-880932-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/93b0fbd631df/fmicb-13-880932-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/04977544cce1/fmicb-13-880932-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/a2e25c18a890/fmicb-13-880932-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/f8214abdc4af/fmicb-13-880932-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c72e/9178343/f704a23ead58/fmicb-13-880932-g0007.jpg

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