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|Title:||Enterococcus faecalis Promotes Innate Immune Suppression and Polymicrobial Catheter-Associated Urinary Tract Infection||Authors:||Tien, Brenda Yin Qi
Goh, Hwee Mian Sharon
Chong, Kelvin Kian Long
Ingersoll, Molly A.
Williams, Rohan B. H.
Kline, Kimberly A.
|Issue Date:||2017||Source:||Tien, B. Y. Q., Goh, H. M. S., Chong, K. K. L., Bhaduri-Tagore, S., Holec, S., Dress, R., et al. (2017). Enterococcus faecalis Promotes Innate Immune Suppression and Polymicrobial Catheter-Associated Urinary Tract Infection. Infection and Immunity, 85(12), e00378-17-.||Series/Report no.:||Infection and Immunity||Abstract:||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 immune-mediated 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.||URI:||https://hdl.handle.net/10356/86659
|ISSN:||0019-9567||DOI:||10.1128/IAI.00378-17||Rights:||© 2017 American Society for Microbiology (ASM). This paper was published in Infection and Immunity and is made available as an electronic reprint (preprint) with permission of American Society for Microbiology (ASM). The published version is available at: [http://dx.doi.org/10.1128/IAI.00378-17]. One print or electronic copy may be made for personal use only. Systematic or multiple reproduction, distribution to multiple locations via electronic or other means, duplication of any material in this paper for a fee or for commercial purposes, or modification of the content of the paper is prohibited and is subject to penalties under law.||Fulltext Permission:||open||Fulltext Availability:||With Fulltext|
|Appears in Collections:||SCELSE Journal Articles|
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