Journal of Microbial & Biochemical Technology

Investigation of immunopathological mechanism of RD functional genes from Mycobacterium tuberculosis

12^th World Congress on Biotechnology and Microbiology

June 28-29, 2018 | Amsterdam, Netherlands

Xiao LIan Zhang, Lingyun Zhang and Huan Xiong

Wuhan University, China

Posters & Accepted Abstracts: J Microb Biochem Technol

Abstract:

Tuberculosis (TB) is a major global health problem. Overall, approximately one-third of the worldâ??s population is currently asymptomatically infected with Mycobacterium tuberculosis (M. tb), the etiological agent of TB. In recent years, comparative genomic studies using subtractive DNA hybridization and DNA microarray have identified >100 open reading frames (ORFs) distributed in several M. tb-specific genomic regions of difference, designated RD1 to RD16. These are absent in BCG and M. bovis, suggesting that the RD-encoded proteins may be virulent factors for TB pathogenicity and associated immune responses. Here after screening RDs recombinant proteins, we found a Rv3873 recombinant protein from RD1 could induce early and late apoptosis in mouse peritoneal macrophages. Rv3873 caused macrophages death independent of TLR2/4, MYD88 and IL-6. Using GST-Pulldown, Mass Spectrometry and Western blot experiments; we found that Rv3873 interacted with H2A protein of macrophages. Dual luciferase reporter assay and western blot assay showed that Rv3873 could down regulate the NF-kappa B transcription, inhibit the phosphorylationâ??s of p-P65, p-JNK and p-ERK, thus further inhibited macrophage early (15-60 minutes) expression of inflammatory factor TNF-alpha. TNF-alpha is an important immune regulatory molecule in anti-tuberculosis immune response. Our data suggest that the inhibition of the expression of TNF-alpha by Rv3873 may promote the progression of tuberculosis. Rv3873 may be as a negative immune regulate factor contributing to TB pathogenesis.