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Recognition of Host Immune Activation by Pseudomonas aeruginosa
Licheng Wu,1Oscar Estrada,1Olga Zaborina,1Manjeet Bains,4Le Shen,2Jonathan E. Kohler,1Nachiket Patel,1Mark W. Musch,3Eugene B. Chang,3Yang-Xin Fu,2Michael A. Jacobs,5Michael I. Nishimura,1Robert E. W. Hancock,4Jerrold R. Turner,2John C. Alverdy1*
It is generally reasoned that lethal infections caused by opportunisticpathogens develop permissively by invading a host that is bothphysiologically stressed and immunologically compromised. However,an alternative hypothesis might be that opportunistic pathogensactively sense alterations in host immune function and respondby enhancing their virulence phenotype. We demonstrate thatinterferon- binds to an outer membrane protein in Pseudomonasaeruginosa, OprF, resulting in the expression of a quorum-sensingdependent virulence determinant, the PA-I lectin. These observationsprovide details of the mechanisms by which prokaryotic organismsare directly signaled by immune activation in their eukaryotichost.
1 Department of Surgery, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA. 2 Department of Pathology, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA. 3 Department of Medicine, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA. 4 Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC V6T1Z4, Canada. 5 Department of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
* To whom correspondence should be addressed. E-mail: jalverdy{at}surgery.bsd.uchicago.edu
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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. 
