Enterococcus faecalis promotes innate immune suppression and polymicrobial catheter-associated urinary tract infection

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Enterococcus faecalis promotes innate immune suppression and polymicrobial catheter-associated urinary tract infection
Title:
Enterococcus faecalis promotes innate immune suppression and polymicrobial catheter-associated urinary tract infection
Other Titles:
Infection and Immunity
Keywords:
Publication Date:
17 November 2017
Citation:
n Tien BYQ, Goh HMS, Chong KKL, Bhaduri-Tagore S, Holec S, Dress R, Ginhoux F, Ingersoll MA, Williams RBH, Kline KA. 2017. Enterococcus faecalis promotes innate immune suppression and polymicrobial catheterassociated urinary tract infection. Infect Immun 85:e00378-17. https://doi.org/10.1128/IAI .00378-17.
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 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-B 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-B-driven responses in macrophages promotes polymicrobial CAUTI pathogenesis, especially during coinfection with less virulent or commensal E. coli strains.
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Funding Info:
B.Y.Q.T., H.M.S.G., K.K.L.C., S.B.-T., S.H., R.B.H.W., and K.A.K. were supported by the National Research Foundation and the Ministry of Education Singapore under its Research Centre of Excellence Programme. B.Y.Q.T., H.M.S.G., K.K.L.C., S.B.-T., S.H., and K.A.K. were supported by the National Research Foundation under its Singapore NRF fellowship program (grant NRF-NRFF2011-11) and by the Ministry of Education Singapore under its tier 2 program (grant MOE2014-T2-1-129). K.A.K. and M.A.I. were supported by the Merlion Programme, sponsored by the French Ministry of Foreign Affairs and Nanyang Technological University. F.G. and R.D. were supported by Singapore Immunology Network core funding from the Agency for Science, Technology and Research (A*STAR), Singapore
Description:
The full paper is available for download at the publisher's URL: https://doi.org/10.1128/IAI.00378-17
ISSN:
0019-9567
1098-5522
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