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

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

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ASJC Scopus subject areas

  • Immunology

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