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FaeG的缺失减轻了产肠毒素大肠杆菌F4ac诱导的肠道细胞凋亡。

Deletion of FaeG alleviated Enterotoxigenic Escherichia coli F4ac-induced apoptosis in the intestine.

作者信息

Xia Pengpeng, Wu Yunping, Lian Siqi, Quan Guomei, Wang Yiting, Zhu Guoqiang

机构信息

College of Veterinary Medicine (Institute of Comparative Medicine), Yangzhou University, Yangzhou 12th East Wenhui Road, Yangzhou, 225009, China.

Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, 225009, China.

出版信息

AMB Express. 2021 Mar 18;11(1):44. doi: 10.1186/s13568-021-01201-z.

Abstract

Enterotoxigenic Escherichia coli (ETEC) F4ac is a major constraint to the development of the pig industry, which is causing newborn and post-weaning piglets diarrhea. Previous studies proved that FaeG is the major fimbrial subunit of F4ac E. coli and efficient for bacterial adherence and receptor recognition. Here we show that the faeG deletion attenuates both the clinical symptoms of F4ac infection and the F4ac-induced intestinal mucosal damage in piglets. Antibody microarray analysis and the detection of mRNA expression using porcine neonatal jejunal IPEC-J2 cells also determined that the absence of FaeG subunit alleviated the F4ac promoted apoptosis in the intestinal epithelial cells. Thus, targeted depletion of FaeG is still beneficial for the prevention or treatment of F4ac infection.

摘要

产肠毒素大肠杆菌(ETEC)F4ac是养猪业发展的主要制约因素,它会导致新生仔猪和断奶后仔猪腹泻。先前的研究证明,FaeG是F4ac大肠杆菌的主要菌毛亚基,对细菌黏附和受体识别有效。在此我们表明,faeG缺失可减轻F4ac感染的临床症状以及F4ac诱导的仔猪肠道黏膜损伤。使用猪新生空肠IPEC-J2细胞进行的抗体微阵列分析和mRNA表达检测还确定,FaeG亚基的缺失减轻了F4ac促进的肠道上皮细胞凋亡。因此,靶向去除FaeG对预防或治疗F4ac感染仍然有益。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbaf/7973317/eb44889afbbc/13568_2021_1201_Fig1_HTML.jpg

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