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Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion.

Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Research Abstract Details 

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  • Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Abstract Text:

    linoj p samuelLinoj P Samuel,chang-hwa songChang-Hwa Song,jun weiJun Wei,esteban a robertsEsteban A Roberts,john l dahlJohn L Dahl,clifton e barryClifton E Barry,eun-kyeong joEun-Kyeong Jo,richard l friedmanRichard L Friedman,

    The eis gene of Mycobacterium tuberculosis has been shown to play a role in the survival of the avirulent Mycobacterium smegmatis within the macrophage. In vitro and in vivo analysis of Deltaeis deletion mutants and complemented strains showed no effect on survival of M. tuberculosis in U-937 macrophages or in a mouse aerosol infection model, respectively. Further studies were done in an attempt to determine the role of eis in M. tuberculosis intracellular survival and to define a phenotypic difference between wild-type and the Deltaeis deletion mutant. Bioinformatic analysis indicated that Eis is an acetyltransferase of the GCN5-related family of N-acetyltransferases. Immunofluorescence microscopy and Western blot analysis studies demonstrated that Eis is released into the cytoplasm of M. tuberculosis-infected U-937 macrophages. Eis was also found in the extravesicular fraction and culture supernatant of M. tuberculosis-infected macrophages. The effect of Eis on human macrophage cytokine secretion was also examined. Eis modulated the secretion of IL-10 and TNF-alpha by primary human monocytes in response both to infection with M. tuberculosis and to stimulation with recombinant Eis protein. These results suggest that Eis is a mycobacterial effector that is released into the host cell to modulate inflammatory responses, possibly via transcriptional or post-translational means.

    Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Publishing Authors By Initials

    lp samuelLP Samuel,ch songCH Song,j weiJ Wei,ea robertsEA Roberts,jl dahlJL Dahl,ce barryCE Barry,ek joEK Jo,rl friedmanRL Friedman,

    For similar biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: virulence research abstracts see: biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: virulence research

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    Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Microbiology (Reading, England)

    VOLUME: 153

    Page Numbers: 529-40

    Journal Abbreviation: Microbiology (Reading, Engl.)

    ISSN: 1350-0872

    DAY: 3

    MONTH: Feb

    YEAR: 2007

    Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9430468

    Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Keywords Mesh Terms:

    KEYWORDS: Virulence

    MESH TERMS: pathogenicity

    Chemical & Substance for Abstract: Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. Information

    Substance Name: Acetyltransferases

    Registry Number: EC 2.3.1.-

    Grant and Affiliation Information for Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion.

    AFFILIATION: Department of Microbiology and Immunology, University of Arizona, Tucson, AZ 85724, USA. Linoj_Samuel@urmc.rochester.edu

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NIAID

    GRANT: AI45537-01A2

    ACRONYM: AI

    MEDLINETA: Microbiology

    REFSOURCE:

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