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StdA 在肠炎沙门氏菌血清型 8 噬菌体黏附宿主肠上皮细胞中的作用。

Role of StdA in adhesion of Salmonella enterica serovar Enteritidis phage type 8 to host intestinal epithelial cells.

机构信息

Department of Animal Sciences, University of Wisconsin-Madison, 1675 Observatory Drive, Madison, WI 53706, USA.

出版信息

Gut Pathog. 2013 Dec 24;5(1):43. doi: 10.1186/1757-4749-5-43.

DOI:10.1186/1757-4749-5-43
PMID:24367906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3877977/
Abstract

BACKGROUND

Salmonella is often implicated in foodborne outbreaks, and is a major public health concern in the United States and throughout the world. Salmonella enterica serovar Enteritidis (SE) infection in humans is often associated with the consumption of contaminated poultry products. Adhesion to epithelial cells in the intestinal mucosa is a major pathogenic mechanism of Salmonella in poultry. Transposon mutagenesis identified stdA as a potential adhesion mutant of SE. Therefore, we hypothesize StdA plays a significant role in adhesion of SE to the intestinal mucosa of poultry.

METHODS AND RESULTS

To test our hypothesis, we created a mutant of SE in which stdA was deleted. Growth and motility were assayed along with the in vitro and in vivo adhesion ability of the ∆stdA when compared to the wild-type SE strain. Our data showed a significant decrease in motility in ∆stdA when compared to the wild-type and complemented strain. A decrease in adhesion to intestinal epithelial cells as well as in the small intestine and cecum of poultry was observed in ∆stdA. Furthermore, the lack of adhesion correlated to a defect in invasion as shown by a cell culture model using intestinal epithelial cells and bacterial recovery from the livers and spleens of chickens.

CONCLUSIONS

These studies suggest StdA is a major contributor to the adhesion of Salmonella to the intestinal mucosa of poultry.

摘要

背景

沙门氏菌常与食源性疾病暴发有关,是美国和全球主要的公共卫生关注点。人类感染肠炎沙门氏菌(SE)通常与食用受污染的家禽产品有关。黏附在肠黏膜上皮细胞是沙门氏菌在禽类中主要的致病机制。转座子诱变鉴定出 stdA 是 SE 的一个潜在黏附突变体。因此,我们假设 StdA 在 SE 黏附禽类肠黏膜中发挥重要作用。

方法与结果

为了验证我们的假设,我们构建了 SE 的 stdA 缺失突变体。与野生型 SE 菌株相比,我们检测了该突变体的生长和运动能力以及体外和体内黏附能力。与野生型和互补菌株相比,我们的数据显示突变体 ∆stdA 的运动能力显著下降。观察到 ∆stdA 对肠道上皮细胞以及禽类小肠和盲肠的黏附能力下降。此外,缺乏黏附能力与侵袭缺陷相关,这通过使用肠上皮细胞的细胞培养模型和从鸡的肝脏和脾脏中回收细菌得到证实。

结论

这些研究表明,StdA 是沙门氏菌黏附禽类肠黏膜的主要因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/33933ec34998/1757-4749-5-43-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/d4e3c6147ee0/1757-4749-5-43-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/c30a800c233c/1757-4749-5-43-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/af51204466d1/1757-4749-5-43-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/43c3075cf8f8/1757-4749-5-43-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/33933ec34998/1757-4749-5-43-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/d4e3c6147ee0/1757-4749-5-43-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/c30a800c233c/1757-4749-5-43-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/af51204466d1/1757-4749-5-43-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/43c3075cf8f8/1757-4749-5-43-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab31/3877977/33933ec34998/1757-4749-5-43-5.jpg

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