ArticleMolecular and cellular biochemistry2010
Expression of PE_PGRS 62 protein in Mycobacterium smegmatis decrease mRNA expression of proinflammatory cytokines IL-1beta, IL-6 in macrophages.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 34 citations in OpenAlex.
- Evolution of the PE_PGRS Proteins of Mycobacteria: Are All Equal or Are Some More Equal than Others?Biology · 2025Review
- Mycobacterium tuberculosis PE_PGRS45 (Rv2615c) Promotes Recombinant Mycobacteria Intracellular Survival via Regulation of Innate Immunity, and Inhibition of Cell Apoptosis.Journal of microbiology (Seoul, Korea) · 2024Article
- Mycobacterial protein PE_PGRS30 induces macrophage apoptosis through prohibitin 2 mitochondrial function interference.Frontiers in microbiology · 2023Article
- PE_PGRS38 Interaction With HAUSP Downregulates Antimycobacterial Host DefenseFrontiers in immunology · 2022Article
- PGRS Domain of Rv0297 ofInternational journal of molecular sciences · 2021Article
- Mycobacterium tuberculosis PE_PGRS41 Enhances the Intracellular Survival of M. smegmatis within Macrophages Via Blocking Innate Immunity and Inhibition of Host Defense.Scientific reports · 2017Article
- Much More than M1 and M2 Macrophages, There are also CD169(+) and TCR(+) Macrophages.Frontiers in immunology · 2015Review
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- Mycobacterium tuberculosis PE_PGRS17 promotes the death of host cell and cytokines secretion via Erk kinase accompanying with enhanced survival of recombinant Mycobacterium smegmatis.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013Article
- Function prediction and analysis of mycobacterium tuberculosis hypothetical proteins.International journal of molecular sciences · 2012Article
- The Mycobacterium tuberculosis PE proteins Rv0285 and Rv1386 modulate innate immunity and mediate bacillary survival in macrophages.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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