Vancomycin-resistant enterococci exploit antibiotic-induced innate immune deficits

Katharina Brandl, George Plitas, Coralia N. Mihu, Carles Ubeda, Ting Jia, Martin Fleisher, Bernd Schnabl, Ronald P. DeMatteo and Eric G. Pamer ()
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Katharina Brandl: Infectious Diseases Service, Immunology Program, Sloan-Kettering Institute
George Plitas: Hepatobiliary Service,
Coralia N. Mihu: Infectious Diseases Service, Immunology Program, Sloan-Kettering Institute
Carles Ubeda: Infectious Diseases Service, Immunology Program, Sloan-Kettering Institute
Ting Jia: Infectious Diseases Service, Immunology Program, Sloan-Kettering Institute
Martin Fleisher: Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
Bernd Schnabl: Columbia University, New York, New York 10032, USA
Ronald P. DeMatteo: Hepatobiliary Service,
Eric G. Pamer: Infectious Diseases Service, Immunology Program, Sloan-Kettering Institute

Nature, 2008, vol. 455, issue 7214, 804-807

Abstract: Antibiotic-resistant bacteria: why are they so successful? Why antibiotic-resistant bacteria are so successful at causing infections in patients being treated with antibiotics is a something of a mystery. One previously unrecognized factor is reported in this issue: treatment with the broad-spectrum antibiotic vancomycin increases infection with resistant bacteria by compromising intestinal innate immunity. In mice receiving the antibiotic, intestinal expression of the antimicrobial protein, RegIIIγ was suppressed. RegIIIγ is notably effective against vancomycin-resistant Enterococcus (VRE), a common infection in hospitalized patients. Therapies that increase levels of this protein, such as orally administered lipopolysaccharide, may therefore be of use in patients receiving broad-spectrum antibiotics.

Date: 2008
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DOI: 10.1038/nature07250

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