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Human milk oligosaccharides protect bladder epithelial cells against uropathogenic E. coli and Streptococcus agalactiae infections (38.5)
Author(s) -
Lin Ann,
Autran Chloe,
Espanola Sophia,
Lewis Amanda,
Bode Lars,
Nizet Victor
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.38.5
Subject(s) - streptococcus agalactiae , microbiology and biotechnology , sialic acid , group b , urinary system , antimicrobial , biology , streptococcus , immunology , medicine , bacteria , genetics
Urinary tract infection (UTI) is primarily caused by uropathogenic E. coli (UPEC) and sometimes Streptococcus agalactiae (GBS). Recurrent infection that can progress to life‐threatening renal failure has remained as a serious global health concern in infants. Human milk oligosaccharides (HMOs) have been detected in urine of breast‐fed, but not formula‐fed neonates. We investigated the antimicrobial properties and mechanisms HMOs deploy to elicit protection in human bladder epithelial cells. We found HMO‐pretreated epithelial cells were significantly more resistant to invasion by UPEC CFT073, a prototypic strain causing urosepsis. However, HMO pre‐treatment had no significant effect in interfering with UPEC adhesion. Conversely, HMO pre‐treated cells suffer significantly less GBS COH‐1 adhesion and invasion. This result was recapitulated in vivo, in which significantly less GBS was recovered from the bladder of mice treated with HMOs. While HMOs do not play a role in maintaining host cell viability during GBS infection, we found HMOs treatment rapidly UPEC‐mediated host cell cytotoxicity. Moreover, the sialic acid‐containing fraction of HMOs reduced UPEC‐mediated MAPK and NF‐κB activation. Collectively, we showed that HMOs protect the urinary tract from microbial infection, and may be a contributing mechanism underlying the epidemiological evidence of reduced UTI incidence in breast‐fed infants. Grant Funding Source : Canadian Institutes of Health Research (CIHR)