Journal
SCIENCE
Volume 309, Issue 5735, Pages 774-777Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1112422
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Funding
- NIDDK NIH HHS [DK-47722, DK-38510, R01DK68271, R01DK61931] Funding Source: Medline
- NIGMS NIH HHS [2-RO1 GM062344-05] Funding Source: Medline
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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-1 lectin. These observations provide details of the mechanisms by which prokaryotic organisms are directly signaled by immune activation in their eukaryotic host.
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