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

Linoj P. Samuel, Chang Hwa Song, Jun Wei, Esteban A. Roberts, John L. Dahl, Clifton E. Barry, Eun Kyeong Jo, Richard L Friedman

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

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 Δeis 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 Δeis 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-α 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.

Original languageEnglish (US)
Pages (from-to)529-540
Number of pages12
JournalMicrobiology
Volume153
Issue number2
DOIs
StatePublished - Feb 2007

Fingerprint

Mycobacterium tuberculosis
Macrophages
Cytokines
Infection
Acetyltransferases
Survival
Mycobacterium smegmatis
Computational Biology
Aerosols
Fluorescence Microscopy
Recombinant Proteins
Interleukin-10
Mycobacterium tuberculosis Eis protein
Monocytes
Cytoplasm
Western Blotting
Genes

ASJC Scopus subject areas

  • Microbiology

Cite this

Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. / Samuel, Linoj P.; Song, Chang Hwa; Wei, Jun; Roberts, Esteban A.; Dahl, John L.; Barry, Clifton E.; Jo, Eun Kyeong; Friedman, Richard L.

In: Microbiology, Vol. 153, No. 2, 02.2007, p. 529-540.

Research output: Contribution to journalArticle

Samuel, Linoj P. ; Song, Chang Hwa ; Wei, Jun ; Roberts, Esteban A. ; Dahl, John L. ; Barry, Clifton E. ; Jo, Eun Kyeong ; Friedman, Richard L. / Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion. In: Microbiology. 2007 ; Vol. 153, No. 2. pp. 529-540.
@article{8c585478fb084738979e17c6e8fad8a8,
title = "Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion",
abstract = "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 Δeis 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 Δeis 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-α 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.",
author = "Samuel, {Linoj P.} and Song, {Chang Hwa} and Jun Wei and Roberts, {Esteban A.} and Dahl, {John L.} and Barry, {Clifton E.} and Jo, {Eun Kyeong} and Friedman, {Richard L}",
year = "2007",
month = "2",
doi = "10.1099/mic.0.2006/002642-0",
language = "English (US)",
volume = "153",
pages = "529--540",
journal = "Microbiology",
issn = "1350-0872",
publisher = "Society for General Microbiology",
number = "2",

}

TY - JOUR

T1 - Expression, production and release of the Eis protein by Mycobacterium tuberculosis during infection of macrophages and its effect on cytokine secretion

AU - Samuel, Linoj P.

AU - Song, Chang Hwa

AU - Wei, Jun

AU - Roberts, Esteban A.

AU - Dahl, John L.

AU - Barry, Clifton E.

AU - Jo, Eun Kyeong

AU - Friedman, Richard L

PY - 2007/2

Y1 - 2007/2

N2 - 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 Δeis 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 Δeis 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-α 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.

AB - 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 Δeis 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 Δeis 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-α 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.

UR - http://www.scopus.com/inward/record.url?scp=33847194247&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33847194247&partnerID=8YFLogxK

U2 - 10.1099/mic.0.2006/002642-0

DO - 10.1099/mic.0.2006/002642-0

M3 - Article

C2 - 17259625

AN - SCOPUS:33847194247

VL - 153

SP - 529

EP - 540

JO - Microbiology

JF - Microbiology

SN - 1350-0872

IS - 2

ER -