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肠炎沙门氏菌鼠伤寒血清型的减毒sopB突变体在牛派伊尔氏淋巴集结中的组织分布和宿主趋化因子反应与野生型相同。

The attenuated sopB mutant of Salmonella enterica serovar Typhimurium has the same tissue distribution and host chemokine response as the wild type in bovine Peyer's patches.

作者信息

Reis Bruno P, Zhang Shuping, Tsolis Renée M, Bäumler Andreas J, Adams L Garry, Santos Renato L

机构信息

Departamento de Clínica e Cirurgia Veterinárias, Escola de Veterinária da Universidade Federal de Minas Gerais, 31270-901 Belo Horizonte, MG, Brazil.

出版信息

Vet Microbiol. 2003 Dec 30;97(3-4):269-77. doi: 10.1016/j.vetmic.2003.09.019.

Abstract

Salmonella enterica serovar Typhimurium is an important cause of enteric infections in farm animals and it is one of the most frequent food borne infections worldwide. Serovar Typhimurium lacking the sopB gene is attenuated for induction of host inflammatory response and fluid accumulation into the intestinal lumen, which correlates with clinical diarrhea. SopB is an inositol phosphate phosphatase, but its exact role in the pathogenesis of salmonellosis is still unclear. We employed the bovine ileal ligated loop model to compare the tissue distribution of a sopB mutant and its wild type parent serovar Typhimurium. Sections of the Peyer's patches were histologically processed and immuno-stained for detection of serovar Typhimurium. In addition, samples were processed for transmission electron microscopy, and the profile of expression of host chemokine and cytokine responses was assessed. Ultrastructurally both strains had the same ability to invade intestinal epithelial cells. No differences were detected in the tissue distribution of the sopB mutant and the wild type organism and both strains elicited the same profile of chemokines and pro-inflammatory cytokines. In conclusion, our results indicate that the attenuation of the sopB mutant is associated with pathogenic mechanisms other than invasion and distribution in host intestinal tissues.

摘要

肠炎沙门氏菌鼠伤寒血清型是家畜肠道感染的重要病因,也是全球最常见的食源性感染之一。缺乏sopB基因的鼠伤寒血清型在诱导宿主炎症反应以及肠腔积液方面减弱,这与临床腹泻相关。SopB是一种肌醇磷酸磷酸酶,但其在沙门氏菌病发病机制中的确切作用仍不清楚。我们采用牛回肠结扎环模型比较sopB突变体及其野生型亲本鼠伤寒血清型的组织分布。对派伊尔氏结切片进行组织学处理并进行免疫染色以检测鼠伤寒血清型。此外,对样本进行透射电子显微镜检查,并评估宿主趋化因子和细胞因子反应的表达情况。超微结构上,两种菌株侵入肠上皮细胞的能力相同。在sopB突变体和野生型菌株的组织分布上未检测到差异,且两种菌株引发的趋化因子和促炎细胞因子情况相同。总之,我们的结果表明,sopB突变体的减毒与宿主肠道组织中的侵袭和分布以外的致病机制有关。

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