Human macrophage gamma interferon decreases gene expression but not replication of Mycobacterium tuberculosis

Analysis of the host-pathogen reciprocal influence on transcription in a comparison of strains H37Rv and CMT97

G. Cappelli, P. Volpe, A. Sanduzzi, A. Sacchi, V. Colizzi, F. Mariani

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Mycobacterium tuberculosis is an intracellular pathogen that readily survives and replicates in human macrophages (Mφ). Host cells have developed different mycobactericidal mechanisms, including the production of inflammatory cytokines. The aim of this study was to compare the Mφ response, in terms of cytokine gene expression, to infection with the M. tuberculosis laboratory strain H37Rv and the clinical M. tuberculosis isolate CMT97. Both strains induce the production of interleukin-12 (IL-12) and IL-16 at comparable levels. However, the clinical isolate induces a significantly higher and more prolonged Mφ activation, as shown by reverse transcription-PCR analysis of IL-1β, IL-6, IL-10, transforming growth factor beta, tumor necrosis factor alpha, and gamma interferon (IFN-γ) transcripts. Interestingly, when IFN-γ transcription is high, the number of M. tuberculosis genes expressed decreases and vice versa, whereas no mycobactericidal effect was observed in terms of bacterial growth. Expression of 11 genes was also studied in the two M. tuberculosis strains by infecting resting or activated Mφ and compared to bacterial intracellular survival. In both cases, a peculiar inverse correlation between expression of these genes and multiplication was observed. The number and type of genes expressed by the two strains differed significantly.

Original languageEnglish
Pages (from-to)7262-7270
Number of pages9
JournalInfection and Immunity
Volume69
Issue number12
DOIs
Publication statusPublished - 2001

Fingerprint

Mycobacterium tuberculosis
Macrophages
Gene Expression
Interleukin-16
Cytokines
Interleukin-12
Interleukin-1
Interferon-alpha
Transforming Growth Factor beta
Interleukin-10
Interferons
Genes
Reverse Transcription
Interferon-gamma
Interleukin-6
Tumor Necrosis Factor-alpha
human IFNG protein
Polymerase Chain Reaction
Survival
Growth

ASJC Scopus subject areas

  • Immunology

Cite this

@article{8fb33eb153504eaea21fd72ee8a3c032,
title = "Human macrophage gamma interferon decreases gene expression but not replication of Mycobacterium tuberculosis: Analysis of the host-pathogen reciprocal influence on transcription in a comparison of strains H37Rv and CMT97",
abstract = "Mycobacterium tuberculosis is an intracellular pathogen that readily survives and replicates in human macrophages (Mφ). Host cells have developed different mycobactericidal mechanisms, including the production of inflammatory cytokines. The aim of this study was to compare the Mφ response, in terms of cytokine gene expression, to infection with the M. tuberculosis laboratory strain H37Rv and the clinical M. tuberculosis isolate CMT97. Both strains induce the production of interleukin-12 (IL-12) and IL-16 at comparable levels. However, the clinical isolate induces a significantly higher and more prolonged Mφ activation, as shown by reverse transcription-PCR analysis of IL-1β, IL-6, IL-10, transforming growth factor beta, tumor necrosis factor alpha, and gamma interferon (IFN-γ) transcripts. Interestingly, when IFN-γ transcription is high, the number of M. tuberculosis genes expressed decreases and vice versa, whereas no mycobactericidal effect was observed in terms of bacterial growth. Expression of 11 genes was also studied in the two M. tuberculosis strains by infecting resting or activated Mφ and compared to bacterial intracellular survival. In both cases, a peculiar inverse correlation between expression of these genes and multiplication was observed. The number and type of genes expressed by the two strains differed significantly.",
author = "G. Cappelli and P. Volpe and A. Sanduzzi and A. Sacchi and V. Colizzi and F. Mariani",
year = "2001",
doi = "10.1128/IAI.69.12.7262-7270.2001",
language = "English",
volume = "69",
pages = "7262--7270",
journal = "Infection and Immunity",
issn = "0019-9567",
publisher = "American Society for Microbiology",
number = "12",

}

TY - JOUR

T1 - Human macrophage gamma interferon decreases gene expression but not replication of Mycobacterium tuberculosis

T2 - Analysis of the host-pathogen reciprocal influence on transcription in a comparison of strains H37Rv and CMT97

AU - Cappelli, G.

AU - Volpe, P.

AU - Sanduzzi, A.

AU - Sacchi, A.

AU - Colizzi, V.

AU - Mariani, F.

PY - 2001

Y1 - 2001

N2 - Mycobacterium tuberculosis is an intracellular pathogen that readily survives and replicates in human macrophages (Mφ). Host cells have developed different mycobactericidal mechanisms, including the production of inflammatory cytokines. The aim of this study was to compare the Mφ response, in terms of cytokine gene expression, to infection with the M. tuberculosis laboratory strain H37Rv and the clinical M. tuberculosis isolate CMT97. Both strains induce the production of interleukin-12 (IL-12) and IL-16 at comparable levels. However, the clinical isolate induces a significantly higher and more prolonged Mφ activation, as shown by reverse transcription-PCR analysis of IL-1β, IL-6, IL-10, transforming growth factor beta, tumor necrosis factor alpha, and gamma interferon (IFN-γ) transcripts. Interestingly, when IFN-γ transcription is high, the number of M. tuberculosis genes expressed decreases and vice versa, whereas no mycobactericidal effect was observed in terms of bacterial growth. Expression of 11 genes was also studied in the two M. tuberculosis strains by infecting resting or activated Mφ and compared to bacterial intracellular survival. In both cases, a peculiar inverse correlation between expression of these genes and multiplication was observed. The number and type of genes expressed by the two strains differed significantly.

AB - Mycobacterium tuberculosis is an intracellular pathogen that readily survives and replicates in human macrophages (Mφ). Host cells have developed different mycobactericidal mechanisms, including the production of inflammatory cytokines. The aim of this study was to compare the Mφ response, in terms of cytokine gene expression, to infection with the M. tuberculosis laboratory strain H37Rv and the clinical M. tuberculosis isolate CMT97. Both strains induce the production of interleukin-12 (IL-12) and IL-16 at comparable levels. However, the clinical isolate induces a significantly higher and more prolonged Mφ activation, as shown by reverse transcription-PCR analysis of IL-1β, IL-6, IL-10, transforming growth factor beta, tumor necrosis factor alpha, and gamma interferon (IFN-γ) transcripts. Interestingly, when IFN-γ transcription is high, the number of M. tuberculosis genes expressed decreases and vice versa, whereas no mycobactericidal effect was observed in terms of bacterial growth. Expression of 11 genes was also studied in the two M. tuberculosis strains by infecting resting or activated Mφ and compared to bacterial intracellular survival. In both cases, a peculiar inverse correlation between expression of these genes and multiplication was observed. The number and type of genes expressed by the two strains differed significantly.

UR - http://www.scopus.com/inward/record.url?scp=0035191662&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035191662&partnerID=8YFLogxK

U2 - 10.1128/IAI.69.12.7262-7270.2001

DO - 10.1128/IAI.69.12.7262-7270.2001

M3 - Article

VL - 69

SP - 7262

EP - 7270

JO - Infection and Immunity

JF - Infection and Immunity

SN - 0019-9567

IS - 12

ER -