Mycobacterium tuberculosis beijing genotype induces differential cytokine production by peripheral blood mononuclear cells of healthy BCG vaccinated individuals

Araceli Rivera-Ordaz, Job Gonzaga-Bernachi, Jeanet Serafn-López, Rogelio Hernández-Pando, Dick Van Soolingen, Sergio Estrada-Parra, Iris Estrada-García, Rommel Chacón-Salinas

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Members of the Mycobacterium tuberculosis (Mtb) Beijing genotype are a major concern due to their high prevalence in tuberculosis patients and their high rate of multi-drug resistance. Although it has been shown that Beijing modifies macrophage behavior, little is known about how this genotype could affect the cellular immune response. In order to address this issue, peripheral blood mononuclear cells (PBMC) from healthy BCG vaccinated individuals were stimulated with protein extracts from three Mycobacterium tuberculosis genotypes: Canetti, H37Rv and Beijing evaluating T cell proliferation and cytokine production. In this system both CD4+ and CD8+ proliferated in a similar manner independently of the Mtb genotype used for stimulation. Regarding cytokines, all strains induced similar levels of IFN-γ, but were unable to induce IL-4 and TGF-β. Contrasting, Canetti strain induced lower production of IL-10, TNF-α and IL-12 compared to H37Rv and Beijing. Interestingly, PBMC stimulated with the Beijing strain produced the highest levels of IL-12 and IL-10 than those stimulated with other strains. This differential cytokine expression could affect the pathogenesis induced by Beijing strain through the modulation of inflammatory process in the host, but the precise mechanisms by which this cytokine environment affects the Beijing strain pathogenesis needs further characterization.

Original languageEnglish
Pages (from-to)144-156
Number of pages13
JournalImmunological Investigations
Volume41
Issue number2
DOIs
StatePublished - Feb 2012

Keywords

  • Beijing strain
  • Cytokine expression
  • Mycobacterium tuberculosis
  • T cell response

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