Enterococcus faecalis promotes innate immune suppression and polymicrobial catheterassociated urinary tract infection

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

Résultats de recherche: Contribution à un journalArticleRevue par des pairs

76 Citations (Scopus)

Résumé

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

langue originaleAnglais
Numéro d'articlee00378-17
journalInfection and Immunity
Volume85
Numéro de publication12
Les DOIs
étatPublié - 1 janv. 2017
Modification externeOui

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