Differential expression of miRNAs by macrophages infected with virulent and avirulent Mycobacterium tuberculosis

Das, Kishore; Saikolappan, Sankaralingam; Dhandayuthapani, Subramanian

doi:10.1016/s1472-9792(13)70010-6

Cited by 55 publications

(45 citation statements)

References 36 publications

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“…We observed a converse expression of miR-30a-5p in isolated aneurysmal M1 and M2 macrophages. Recently, it was shown that miR-30a-5p with eight others was differently expressed in THP-1 macrophages in response to infectious agent such as M. tuberculosis [29] and regulated suppressor of cytokine signaling 3 in ApoE −/− mice, which is implicated in the anti-apoptotic pathway [30]. In contrast, miR-15a-3p was similarly regulated in the isolated aneurysmal cells tested as well in the whole aorta.…”

Section: Resultsmentioning

confidence: 99%

Adventitial Tertiary Lymphoid Organs as Potential Source of MicroRNA Biomarkers for Abdominal Aortic Aneurysm

Spear

Boytard

Blervaque

et al. 2015

IJMS

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Abdominal aortic aneurysm (AAA) is an inflammatory disease associated with marked changes in the cellular composition of the aortic wall. This study aims to identify microRNA (miRNA) expression in aneurysmal inflammatory cells isolated by laser microdissection from human tissue samples. The distribution of inflammatory cells (neutrophils, B and T lymphocytes, mast cells) was evaluated in human AAA biopsies. We observed in half of the samples that adventitial tertiary lymphoid organs (ATLOs) with a thickness from 0.5 to 2 mm were located exclusively in the adventitia. Out of the 850 miRNA that were screened by microarray in isolated ATLOs (n = 2), 164 miRNAs were detected in ATLOs. The three miRNAs (miR-15a-3p, miR-30a-5p and miR-489-3p) with the highest expression levels were chosen and their expression quantified by RT-PCR in isolated ATLOs (n = 4), M1 (n = 2) and M2 macrophages (n = 2) and entire aneurysmal biopsies (n = 3). Except for the miR-30a-5p, a similar modulation was found in ATLOs and the two subtypes of macrophages. The modulated miRNAs were then evaluated in the plasma of AAA patients for their potential as AAA biomarkers. Our data emphasize the potential of miR-15a-3p and miR-30a-5p as biomarkers of AAA but also as triggers of ATLO evolution. Further investigations will be required to evaluate their targets in order to better understand AAA pathophysiology.

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Section: Resultsmentioning

confidence: 99%

Adventitial Tertiary Lymphoid Organs as Potential Source of MicroRNA Biomarkers for Abdominal Aortic Aneurysm

Spear

Boytard

Blervaque

et al. 2015

IJMS

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“…M. tuberculosis is an ancient organism that has coevolved with its human host; therefore, it is uniquely adapted for survival within its intracellular host: the macrophage (36). To date, little data exist on how miRNAs alter human macrophage immune responses during infection, which are the first phagocyte immune responders to M. tuberculosis in the lung microenvironment (37). This study emphasizes the effects of primary M. tuberculosis infection, which determines the outcome of active or latent infection, on macrophage miRNAs using a pure primary human macrophage model of tuberculosis.…”

Section: Discussionmentioning

confidence: 99%

Mycobacterium tuberculosisDecreases Human Macrophage IFN-γ Responsiveness through miR-132 and miR-26a

Rajaram

Lafuse

et al. 2014

The Journal of Immunology

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IFN-γ–activated macrophages play an essential role in controlling intracellular pathogens; however, macrophages also serve as the cellular home for the intracellular pathogen Mycobacterium tuberculosis. Based on previous evidence that M. tuberculosis can modulate host microRNA (miRNA) expression, we examined the miRNA expression profile of M. tuberculosis–infected primary human macrophages. We identified 31 differentially expressed miRNAs in primary human macrophages during M. tuberculosis infection by NanoString and confirmed our findings by quantitative real-time RT-PCR. In addition, we determined a role for two miRNAs upregulated upon M. tuberculosis infection, miR-132 and miR-26a, as negative regulators of transcriptional coactivator p300, a component of the IFN-γ signaling cascade. Knockdown expression of miR-132 and miR-26a increased p300 protein levels and improved transcriptional, translational, and functional responses to IFN-γ in human macrophages. Collectively, these data validate p300 as a target of miR-132 and miR-26a, and demonstrate a mechanism by which M. tuberculosis can limit macrophage responses to IFN-γ by altering host miRNA expression.

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“…Indeed, in infected macrophages, miRNAs are differentially expressed between virulent and avirulent Mtb [27], between the highly virulent Beijing/W strains nonBeijing/W clinical strains [28], and deep sequencing analysis of multidrug-resistant (MDR) Mtb strains revealed that miRNAs were differentially expressed compared to antibiotic sensitive Mtb strains [29]. Upon contact with the host, pathogenic bacteria induce a sequence of mechanisms to promote its invasion and the establishment of a successful infection within the host.…”

Section: Immunomodulating Micrornas Of Mycobacterial Infectionsmentioning

confidence: 99%

Immunomodulating microRNAs of mycobacterial infections

2016

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Differential expression of miRNAs by macrophages infected with virulent and avirulent Mycobacterium tuberculosis

Cited by 55 publications

References 36 publications

Adventitial Tertiary Lymphoid Organs as Potential Source of MicroRNA Biomarkers for Abdominal Aortic Aneurysm

Adventitial Tertiary Lymphoid Organs as Potential Source of MicroRNA Biomarkers for Abdominal Aortic Aneurysm

Mycobacterium tuberculosisDecreases Human Macrophage IFN-γ Responsiveness through miR-132 and miR-26a

Immunomodulating microRNAs of mycobacterial infections

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