Expression of PE_PGRS 62 protein in Mycobacterium smegmatis decrease mRNA expression of proinflammatory cytokines IL-1beta, IL-6 in macrophages

Mol Cell Biochem. 2010 Jul;340(1-2):223-9. doi: 10.1007/s11010-010-0421-x. Epub 2010 Mar 11.

Abstract

The pathogenesis of tuberculosis causing Mycobacterium bovis is largely due to its successful entry and survival in macrophages. Previous research indicated that mycobacteria-specific PE_PGRS genes code for cell surface proteins which may have role in mediating interactions with macrophages. In this study, we expressed PE_PGRS 62 gene in a non-pathogenic fast growing Mycobacterium smegmatis strain and found that the recombinant Mycobacterium smegmatis decreased macrophages livability in a dosage-dependent manner and time-dependent manner, compared with parental strain containing the vector only. To explore whether PE_PGRS 62 modulates the gene expression profile of macrophages, we stimulated macrophages by the M. smegmatis strain expressing PE_PGRS 62 as well as the control strains, followed by real-time RT-PCR assay for the mRNA expression level of IL-1beta, IL-6, and iNOS. The results showed that the expression of IL-1beta, IL-6 in macrophages were down-regulated by stimulation with the M. smegmatis strain expressing PE_PGRS 62 compared to the control strains (P < 0.05). In contrast, there were no measurable differences in the expression of iNOS. Overall, we demonstrated that PE_PGRS 62 protein altered the immune environment of the host cells, which suggest that the pathogenic PE_PGRS 62 protein altering the immune mechanism maybe involved in the pathogenesis of mycobacterial disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Bacterial / genetics
  • Antigens, Bacterial / metabolism*
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism*
  • Cell Line
  • Down-Regulation
  • Gene Expression Regulation, Bacterial
  • Inflammation Mediators / metabolism*
  • Interleukin-1beta / genetics*
  • Interleukin-6 / genetics*
  • Macrophages / immunology*
  • Macrophages / microbiology
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Mycobacterium smegmatis / genetics
  • Mycobacterium smegmatis / immunology*
  • Nitric Oxide Synthase Type II / genetics
  • RNA, Messenger / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors

Substances

  • Antigens, Bacterial
  • Bacterial Proteins
  • Inflammation Mediators
  • Interleukin-1beta
  • Interleukin-6
  • Membrane Proteins
  • PE-PGRS protein, Mycobacterium
  • RNA, Messenger
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse