Abstract
The mechanisms of latent tuberculosis (TB) infection remain elusive. Roles of microRNA (miRNA) have been highlighted in pathogen–host interactions recently. To identify miRNAs involved in the immune response to TB, expression profiles of miRNAs in CD4+ T cells from patients with latent TB, active TB and healthy controls were investigated by microarray assay and validated by RT-qPCR. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used to analyse the significant functions and involvement in signalling pathways of the differentially expressed miRNAs. To identify potential target genes for miR-29, interferon-γ (IFN-γ) mRNA expression was measured by RT-qPCR. Our results showed that 27 miRNAs were deregulated among the three groups. RT-qPCR results were generally consistent with the microarray data. We observed an inverse correlation between miR-29 level and IFN-γ mRNA expression in CD4+ T cells. GO and KEGG pathway analysis showed that the possible target genes of deregulated miRNAs were significantly enriched in mitogen-activated protein kinase signalling pathway, focal adhesion and extracellular matrix receptor interaction, which might be involved in the transition from latent to active TB. In all, for the first time, our study revealed that some miRNAs in CD4+ T cells were altered in latent and active TB. Function and pathway analysis highlighted the possible involvement of miRNA-deregulated mRNAs in TB. The study might help to improve understanding of the relationship between miRNAs in CD4+ T cells and TB, and laid an important foundation for further identification of the underlying mechanisms of latent TB infection and its reactivation.
Highlights
Infection with Mycobacterium tuberculosis (Mtb) can result in active TB or, more commonly latent TB [1]
82 miRNAs were up-regulated and 53 miRNAs were down-regulated in the active TB group compared with the control group (Fig. 1); 33 miRNAs were increased and 46 miRNAs were decreased in the latent TB infection (LTBI) group compared with the control group (Fig. 1); 62 miRNAs were a 2013 The Authors
A recent study reported that 17 miRNAs were differentially expressed in peripheral blood mononuclear cells (PBMCs) from participants with LTBI, active TB and healthy controls a 2013 The Authors
Summary
Infection with Mycobacterium tuberculosis (Mtb) can result in active TB or, more commonly latent TB [1]. About 5–10% of persons with latent TB infection (LTBI) will go on to develop active TB at a later stage of their life [2, 3]. About two billion persons worldwide are estimated to have LTBI, who represent an enormous reservoir of potential reactivation TB cases. Latency is associated with the state in which host is able to control infection, but unable to completely eradicate Mtb [4]. The exact underlying mechanisms of LTBI and its reactivation remain elusive. Further understanding of the mechanisms, by which Mtb establishes a latent state, eludes immune surveillance and responds to reactivation, is crucial for control of TB in the future
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