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Glucuronic acid confers colonization advantage to enteric pathogens

殖民地化 微生物学 毒力 柠檬酸杆菌 殖民抵抗 病菌 葡萄糖醛酸 生物 寄主(生物学) 毒力因子 胃肠道 细菌 大肠杆菌 生物化学 生态学 基因 遗传学 多糖
作者
Thibaut Rosay,Angel G. Jimenez,Vanessa Sperandio
出处
期刊:Proceedings of the National Academy of Sciences of the United States of America [Proceedings of the National Academy of Sciences]
卷期号:121 (13)
标识
DOI:10.1073/pnas.2400226121
摘要

Glucuronidation is a detoxification process to eliminate endo- and xeno-biotics and neurotransmitters from the host circulation. Glucuronosyltransferase binds these compounds to glucuronic acid (GlcA), deactivating them and allowing their elimination through the gastrointestinal (GI) tract. However, the microbiota produces β-glucuronidases that release GlcA and reactivate these compounds. Enteric pathogens such as enterohemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium sense and utilize galacturonic acid (GalA), an isomer of GlcA, to outcompete the microbiota promoting gut colonization. However, the role of GlcA in pathogen colonization has not been explored. Here, we show that treatment of mice with a microbial β-glucuronidase inhibitor (GUSi) decreased C. rodentium ’s colonization of the GI tract, without modulating bacterial virulence or host inflammation. Metagenomic studies indicated that GUSi did not change the composition of the intestinal microbiota in these animals. GlcA confers an advantage for pathogen expansion through its utilization as a carbon source. Congruently mutants unable to catabolize GlcA depict lower GI colonization compared to wild type and are not sensitive to GUSi. Germfree mice colonized with a commensal E. coli deficient for β-glucuronidase production led to a decrease of C. rodentium tissue colonization, compared to animals monocolonized with an E. coli proficient for production of this enzyme. GlcA is not sensed as a signal and doesn’t activate virulence expression but is used as a metabolite. Because pathogens can use GlcA to promote their colonization, inhibitors of microbial β-glucuronidases could be a unique therapeutic against enteric infections without disturbing the host or microbiota physiology.
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