Suppr超能文献

粪肠球菌促进先天性免疫抑制和多微生物导管相关尿路感染。

Enterococcus faecalis Promotes Innate Immune Suppression and Polymicrobial Catheter-Associated Urinary Tract Infection.

作者信息

Tien Brenda Yin Qi, Goh Hwee Mian Sharon, Chong Kelvin Kian Long, Bhaduri-Tagore Soumili, Holec Sarah, Dress Regine, Ginhoux Florent, Ingersoll Molly A, Williams Rohan B H, Kline Kimberly A

机构信息

Singapore Centre for Environmental Life Sciences Engineering, School of Biological Sciences, Nanyang Technological University, Singapore.

Singapore Centre for Environmental Life Sciences Engineering, Interdisciplinary Graduate School, Nanyang Technological University, Singapore.

出版信息

Infect Immun. 2017 Nov 17;85(12). doi: 10.1128/IAI.00378-17. Print 2017 Dec.

Abstract

, a member of the human gastrointestinal microbiota, is an opportunistic pathogen associated with hospital-acquired wound, bloodstream, and urinary tract infections. can subvert or evade immune-mediated clearance, although the mechanisms are poorly understood. In this study, we examined -mediated subversion of macrophage activation. We observed that actively prevents NF-κB signaling in mouse RAW264.7 macrophages in the presence of Toll-like receptor agonists and during polymicrobial infection with and coinfection in a mouse model of catheter-associated urinary tract infection (CAUTI) resulted in a suppressed macrophage transcriptional response in the bladder compared to that with infection alone. Finally, we demonstrated that coinoculation of with a commensal strain of into catheterized bladders significantly augmented CAUTI. Taken together, these results support the hypothesis that suppression of NF-κB-driven responses in macrophages promotes polymicrobial CAUTI pathogenesis, especially during coinfection with less virulent or commensal strains.

摘要

作为人类胃肠道微生物群的一员,是一种与医院获得性伤口、血流和尿路感染相关的机会致病菌。尽管其机制尚不清楚,但它可以颠覆或逃避免疫介导的清除。在本研究中,我们研究了介导的巨噬细胞激活的颠覆。我们观察到,在Toll样受体激动剂存在的情况下,以及在导管相关尿路感染(CAUTI)小鼠模型中与和共感染的多微生物感染期间,能积极阻止小鼠RAW264.7巨噬细胞中的NF-κB信号传导,与单独感染相比,这导致膀胱中巨噬细胞转录反应受到抑制。最后,我们证明,将与共生菌株共同接种到导尿膀胱中可显著增加CAUTI。综上所述,这些结果支持了这样一种假设,即巨噬细胞中NF-κB驱动反应的抑制促进了多微生物CAUTI的发病机制,尤其是在与毒性较小的或共生菌株共感染期间。

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