Analysis of miRNA expression profiling in human macrophages responding to Mycobacterium infection: Induction of the immune regulator miR-146a

Liu, Zhen; Zhou, Guoyong; Deng, Xiangdong; Qi, Yu; Hu, Yongliang; Sun, Haijie; Wang, Zhongyuan; Chen, Hongbing; Jia, Chiyu; Wang, Di

doi:10.1016/j.jinf.2013.12.017

Cited by 57 publications

(64 citation statements)

References 39 publications

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“…Given that many autophagy-related genes are targeted by various microRNAs, it can be concluded that microRNAs play a critical role in autophagy regulation. In our previous report, we have identified non-overlapping signatures of a small number of miRNAs that were aberrantly expressed in MTB infected THP-1 cells and found that the expression level of miR-30A was significantly upregulated (8). In this study, we focused on the regulatory role of miR-30A in autophagy triggered by MTB infection in human macrophage.…”

Section: Discussionmentioning

confidence: 95%

“…The in vitro infection model was established according to our previous report (8). Briefly, THP-1 cells were seeded at a density of 5 × 10 6 cells/flask and grown to 80z confluence.…”

Section: Discussionmentioning

confidence: 99%

“…Alveolar macrophages (AMs) from bronchoalveolar lavage (BAL) of 65 pulmonary tuberculosis (PTB) patients (45 smear-positive and 20 smear-negative) and 15 volunteers were collected from the Hospital of No. 309 of Chinese People's Liberation Army (PLA), as described in our previous report (8) and used for RNA extraction. During the 8-week long treatment, all patients received a short course of 4 anti-tuberculosis drugs, which were administered daily at standard doses (isoniazid, 300 mg; rifampin, 600 mg; pyrazinamide, 1.6 g; and ethambutol, 1.2 g), under the directly observed treatment, short-course strategy, as proposed by the World Health Organization.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of Autophagy by MiR-30A Induced by <i>Mycobacteria tuberculosis</i> as a Possible Mechanism of Immune Escape in Human Macrophages

et al. 2015

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SUMMARY:The regulatory mechanism of miRNA induction in response to Mycobacterium tuberculosis (MTB) infection has not been clearly established. Autophagy has recently been identified as an effective way to control intracellular survival of MTB. In the present study, we demonstrate a novel role of miR-30A in the negative regulation of the autophagy-mediated anti-MTB response. We found that overexpression of miR-30A suppresses the elimination of intracellular MTB through the inhibition of autophagy. Furthermore, there was a negative correlation between concentrations of miR-30A and beclin-1 in MTB positive patients and miR-30A expression decreased after anti-TB treatment. Our results indicate that miR-30A plays a key role in immune response against MTB and, therefore, may serve as a potential target for future treatments of tuberculosis infection.

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Section: Discussionmentioning

confidence: 95%

“…The in vitro infection model was established according to our previous report (8). Briefly, THP-1 cells were seeded at a density of 5 × 10 6 cells/flask and grown to 80z confluence.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibition of Autophagy by MiR-30A Induced by <i>Mycobacteria tuberculosis</i> as a Possible Mechanism of Immune Escape in Human Macrophages

et al. 2015

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“…This study examined the expression of miRs previously reported as suitable to normalise miRNA levels in a variety of biological tissues . The selection of miRs to normalise miRNA is influenced not only by the tissue being examined but also the disease condition being evaluated.…”

Section: Discussionmentioning

confidence: 99%

Identification of miR‐93 as a suitable miR for normalizing miRNA in plasma of tuberculosis patients

Barry

Chan

Ellis

et al. 2015

J Cellular Molecular Medi

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Tuberculosis (TB) remains a major public health issue. New tests to aid diagnoses and monitor the response to therapy are urgently required. There is growing interest in the use of microRNA (miRNA) profiles as diagnostic, prognostic or predictive markers in a range of clinical and infectious diseases, including Mycobacterium tuberculosis infection, however, challenges exist to accurately normalise miRNA levels in cohorts. This study examined the appropriateness of 12 miRs and RNU6B to normalise circulating plasma miRNA levels in individuals with active TB from 2 different geographical and ethnic regions. Twelve miRs (let-7, miR-16, miR-22, miR-26, miR-93, miR-103, miR-191, miR-192, miR-221, miR-423, miR-425 and miR-451) and RNU6B were selected based on their reported production by lung cells, expression in blood and previous use as a reference miRNA. Expression levels were analysed in the plasma of newly diagnosed TB patients from Australia and China compared with individuals with latent TB infection and healthy volunteers. Analysis with both geNorm and NormFinder software identified miR-93 as the most suitable reference miR in both cohorts, either when analysed separately or collectively. Interestingly, there were large variations in the expression levels of some miRs, in particular miR-192 and let-7, between the two cohorts, independent of disease status. These data identify miR-93 is a suitable reference miR for normalizing miRNA levels in TB patients, and highlight how environmental, and possibly ethnic, factors influence miRNA expression levels, demonstrating the necessity of assessing the suitability of reference miRs within the study population.

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“…Also, they found an uncontrolled autoimmune profile in miR-146a −/− knockout mice, as the animals were hyper-responsive to LPS challenge, producing high levels of those pro-inflammatory cytokines TNF, IL-6 [41] that was also in agreement with previous reports [56], [57] and our results here. It was recently shown that M. bovis BCG induces miR-146a expression and regulates TNF levels [58]. In our model, only live M. leprae was able to stimulate miR-146a expression.…”

Section: Discussionmentioning

confidence: 56%

Pre-miR-146a (rs2910164 G>C) Single Nucleotide Polymorphism Is Genetically and Functionally Associated with Leprosy

et al. 2014

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Mycobacterium leprae infects macrophages and Schwann cells inducing a gene expression program to facilitate its replication and progression to disease. MicroRNAs (miRNAs) are key regulators of gene expression and could be involved during the infection. To address the genetic influence of miRNAs in leprosy, we enrolled 1,098 individuals and conducted a case-control analysis in order to study four miRNAs genes containing single nucleotide polymorphism (miRSNP). We tested miRSNP-125a (rs12975333 G>T), miRSNP-223 (rs34952329 *>T), miRSNP-196a-2 (rs11614913 C>T) and miRSNP-146a (rs2910164 G>C). Amongst them, miRSNP-146a was the unique gene associated with risk to leprosy per se (GC OR = 1.44, p = 0.04; CC OR = 2.18, p = 0.0091). We replicated this finding showing that the C-allele was over-transmitted (p = 0.003) using a transmission-disequilibrium test. A functional analysis revealed that live M. leprae (MOI 100∶1) was able to induce miR-146a expression in THP-1 (p<0.05). Furthermore, pure neural leprosy biopsies expressed augmented levels of that miRNA as compared to biopsy samples from neuropathies not related with leprosy (p = 0.001). Interestingly, carriers of the risk variant (C-allele) produce higher levels of mature miR-146a in nerves (p = 0.04). From skin biopsies, although we observed augmented levels of miR-146a, we were not able to correlate it with a particular clinical form or neither host genotype. MiR-146a is known to modulate TNF levels, thus we assessed TNF expression (nerve biopsies) and released by peripheral blood mononuclear cells infected with BCG Moreau. In both cases lower TNF levels correlates with subjects carrying the risk C-allele, (p = 0.0453 and p = 0.0352; respectively), which is consistent with an immunomodulatory role of this miRNA in leprosy.

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Analysis of miRNA expression profiling in human macrophages responding to Mycobacterium infection: Induction of the immune regulator miR-146a

Cited by 57 publications

References 39 publications

Inhibition of Autophagy by MiR-30A Induced by <i>Mycobacteria tuberculosis</i> as a Possible Mechanism of Immune Escape in Human Macrophages

Inhibition of Autophagy by MiR-30A Induced by <i>Mycobacteria tuberculosis</i> as a Possible Mechanism of Immune Escape in Human Macrophages

Identification of miR‐93 as a suitable miR for normalizing miRNA in plasma of tuberculosis patients

Pre-miR-146a (rs2910164 G>C) Single Nucleotide Polymorphism Is Genetically and Functionally Associated with Leprosy

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