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

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

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National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing 100193, People's Republic of China.


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.

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