Microbiology: Recognition of host immune activation by Pseudomonas aeruginosa

Licheng Wu; Oscar Estrada; Olga Zaborina; Manjeet Bains; Le Shen; Jonathan E. Kohler; Nachiket Patel; Mark W. Musch; Eugene B. Chang; Yang Xin Fu; Michael A. Jacobs; Michael I. Nishimura; Robert E.W. Hancock; Jerrold R. Turner; John C. Alverdy

doi:10.1126/science.1112422

Microbiology: Recognition of host immune activation by Pseudomonas aeruginosa

Licheng Wu, Oscar Estrada, Olga Zaborina, Manjeet Bains, Le Shen, Jonathan E. Kohler, Nachiket Patel, Mark W. Musch, Eugene B. Chang, Yang Xin Fu, Michael A. Jacobs, Michael I. Nishimura, Robert E.W. Hancock, Jerrold R. Turner, John C. Alverdy

Research output: Contribution to journal › Article › peer-review

272 Citations (Scopus)

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-γ 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.

Original language	English
Pages (from-to)	774-777
Number of pages	4
Journal	Science
Volume	309
Issue number	5735
DOIs	https://doi.org/10.1126/science.1112422
Publication status	Published or Issued - 29 Jul 2005
Externally published	Yes

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title = "Microbiology: Recognition of host immune activation by Pseudomonas aeruginosa",

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-γ 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.",

author = "Licheng Wu and Oscar Estrada and Olga Zaborina and Manjeet Bains and Le Shen and Kohler, {Jonathan E.} and Nachiket Patel and Musch, {Mark W.} and Chang, {Eugene B.} and Fu, {Yang Xin} and Jacobs, {Michael A.} and Nishimura, {Michael I.} and Hancock, {Robert E.W.} and Turner, {Jerrold R.} and Alverdy, {John C.}",

year = "2005",

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doi = "10.1126/science.1112422",

language = "English",

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TY - JOUR

T1 - Microbiology

T2 - Recognition of host immune activation by Pseudomonas aeruginosa

AU - Wu, Licheng

AU - Estrada, Oscar

AU - Zaborina, Olga

AU - Bains, Manjeet

AU - Shen, Le

AU - Kohler, Jonathan E.

AU - Patel, Nachiket

AU - Musch, Mark W.

AU - Chang, Eugene B.

AU - Fu, Yang Xin

AU - Jacobs, Michael A.

AU - Nishimura, Michael I.

AU - Hancock, Robert E.W.

AU - Turner, Jerrold R.

AU - Alverdy, John C.

PY - 2005/7/29

Y1 - 2005/7/29

N2 - 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-γ 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.

AB - 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-γ 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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VL - 309

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JO - Science

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Microbiology: Recognition of host immune activation by Pseudomonas aeruginosa

Abstract

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