Recognition of Host Immune Activation by <i>Pseudomonas aeruginosa</i>

Licheng Wu(University of British Columbia), Oscar Estrada(University of British Columbia), Olga Zaborina(University of British Columbia), Manjeet Bains(University of British Columbia), Le Shen(University of British Columbia), Jonathan E. Kohler(University of British Columbia), Nachiket Patel(University of British Columbia), Mark W. Musch(University of British Columbia), Eugene B. Chang(University of British Columbia), Yang‐Xin Fu(University of British Columbia), Michael A. Jacobs(University of British Columbia), Michael I. Nishimura(University of British Columbia), Robert E. W. Hancock(University of British Columbia), Jerrold R. Turner(University of British Columbia), John C. Alverdy(University of British Columbia)
Science
July 28, 2005
10.1126/science.1112422
Cited by 322

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.

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