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单宁酸通过靶向Ⅲ型分泌系统抑制鼠伤寒血清型沙门氏菌感染。

Tannic Acid Inhibits Serovar Typhimurium Infection by Targeting the Type III Secretion System.

作者信息

Shu Jingyan, Liu Hongtao, Liu Yang, Chen Xindi, Yu Yu, Lv Qianghua, Wang Jianfeng, Deng Xuming, Guo Zhimin, Qiu Jiazhang

机构信息

Key Laboratory of Zoonosis, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, China.

Department of Clinical Laboratory, The First Hospital of Jilin University, Changchun, China.

出版信息

Front Microbiol. 2022 Jan 25;12:784926. doi: 10.3389/fmicb.2021.784926. eCollection 2021.

DOI:10.3389/fmicb.2021.784926
PMID:35145491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8822118/
Abstract

serovar Typhimurium ( Typhimurium) is a zoonotic pathogen that can cause food poisoning and diarrhea in both humans and animals worldwide. The pathogenicity island (SPI) genes encoded type III secretion system (T3SS) is important for Typhimurium invasion and replication in host cells. Due to the increasing problem of antibiotic resistance, antibiotic treatment for clinical infection has gradually been limited. Anti-virulence inhibitors are a promising alternative to antibiotics because they do not easily induce bacterial antibiotic resistance. Here, we systematically evaluated the therapeutic effect of tannic acid (TA) on infected mice and elucidated its anti-infection mechanism. TA treatment improved the survival rate of Typhimurium-infected mice and alleviated cecum pathological lesions. In addition, TA inhibited Typhimurium invasion to HeLa cells without affecting their growth. Further studies showed that TA could inhibit the expression of and This inhibition may be implemented by inhibiting the transcription of key regulatory and structural genes of the T3SS. This study provides an alternative anti-virulence strategy for infection treatment.

摘要

鼠伤寒血清型沙门氏菌(鼠伤寒沙门氏菌)是一种人畜共患病原体,可在全球范围内导致人类和动物食物中毒及腹泻。致病岛(SPI)基因编码的III型分泌系统(T3SS)对于鼠伤寒沙门氏菌在宿主细胞中的侵袭和复制至关重要。由于抗生素耐药性问题日益严重,临床感染的抗生素治疗逐渐受到限制。抗毒力抑制剂是抗生素的一种有前景的替代物,因为它们不容易诱导细菌产生抗生素耐药性。在此,我们系统地评估了鞣酸(TA)对感染小鼠的治疗效果,并阐明了其抗感染机制。TA治疗提高了鼠伤寒沙门氏菌感染小鼠的存活率,并减轻了盲肠病理损伤。此外,TA抑制鼠伤寒沙门氏菌对HeLa细胞的侵袭,而不影响其生长。进一步研究表明,TA可抑制 和 的表达。这种抑制可能是通过抑制T3SS关键调控基因和结构基因的转录来实现的。本研究为 感染治疗提供了一种替代的抗毒力策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/761e0ba69825/fmicb-12-784926-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/82c32757c62c/fmicb-12-784926-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/d58b1456ae82/fmicb-12-784926-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/3b0a244e2ac7/fmicb-12-784926-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/761e0ba69825/fmicb-12-784926-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/82c32757c62c/fmicb-12-784926-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/d58b1456ae82/fmicb-12-784926-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/3b0a244e2ac7/fmicb-12-784926-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d129/8822118/761e0ba69825/fmicb-12-784926-g004.jpg

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