Abstract
It is generally reasoned that lethal infections caused by opportunistic pathogens develop permissively by invading a host that is both physiologically stressed and immunologically compromised. However, an alternative hypothesis might be that opportunistic pathogens actively sense alterations in host immune function and respond by enhancing their virulence phenotype. We demonstrate that interferon-gamma binds to an outer membrane protein in Pseudomonas aeruginosa, OprF, resulting in the expression of a quorum-sensing dependent virulence determinant, the PA-I lectin. These observations provide details of the mechanisms by which prokaryotic organisms are directly signaled by immune activation in their eukaryotic host.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adhesins, Bacterial / biosynthesis*
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Animals
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Cell Line
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Cell Line, Tumor
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Cells, Cultured
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Cytokines / immunology
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Cytokines / metabolism
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Cytokines / pharmacology
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Humans
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Interferon-gamma / immunology
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Interferon-gamma / metabolism*
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Interferon-gamma / pharmacology
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Lectins / biosynthesis*
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Lymphocyte Activation
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Porins / isolation & purification
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Porins / metabolism*
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Protein Binding
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Pseudomonas aeruginosa / growth & development
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Pseudomonas aeruginosa / immunology*
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Pseudomonas aeruginosa / metabolism
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Pseudomonas aeruginosa / pathogenicity*
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Pyocyanine / biosynthesis
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Recombinant Proteins / pharmacology
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Signal Transduction
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T-Lymphocytes / immunology*
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Up-Regulation
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Virulence
Substances
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Adhesins, Bacterial
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Cytokines
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Lectins
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Porins
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Recombinant Proteins
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adhesin, Pseudomonas
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Interferon-gamma
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Pyocyanine