MicroRNA‑502‑3p promotes <i>Mycobacterium tuberculosis</i> survival in macrophages by modulating the inflammatory response by targeting ROCK1

Liu, Fang; Dong, Zhen; Lin, Yuefu; Yang, Haibo; Wang, Pingping; Zhang, Yongxia

doi:10.3892/mmr.2021.12393

Cited by 6 publications

(6 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…M.tb, Mycobacterium tuberculosis; mRNA, messenger RNA; interleukin 6, IL-6; IL-1β. interleukin 1 β; TNF-α, tumor necrosis factor α; ELISA, enzymelinked immunosorbent assay; IL-10, interleukin 10; SD, standard deviation Consistent with the reported findings, 13,35,36 our project demonstrated that M.tb infection led to the overproduction of proinflammatory factors in THP-1 cells. However, M.tb is able to resist these antimicrobial activities by establishing a niche for survival in macrophages.…”

Section: Discussionsupporting

confidence: 88%

“…The production of inflammatory cytokines by macrophages is regarded as a bactericidal pathway for M.tb infection 34 . Consistent with the reported findings, 13,35,36 our project demonstrated that M.tb infection led to the overproduction of pro‐inflammatory factors in THP‐1 cells. However, M.tb is able to resist these antimicrobial activities by establishing a niche for survival in macrophages 37 .…”

Section: Discussionsupporting

confidence: 85%

“…10 Toll-like receptor 4/nuclear factor-κ B (TLR4/NF-κB) is an important inflammatory signalling pathway in TB. [11][12][13] We aim to explore the effects of hsa_circ_0001204 on macrophage apoptosis and inflammatory response induced by M.tb infection through in vitro cell experiments. The potential regulatory relationship between TLR4/NF-κB signalling pathway and hsa_circ_0001204 in TB was also investigated.…”

Section: Tuberculosis (Tb) Is a Deadly Infectious Disease Mainly Caus...mentioning

confidence: 99%

“…CircRNAs can play a vital role in many diseases by regulating signalling cascades 10 . Toll‐like receptor 4/nuclear factor‐κ B (TLR4/NF‐κB) is an important inflammatory signalling pathway in TB 11–13 . We aim to explore the effects of hsa_circ_0001204 on macrophage apoptosis and inflammatory response induced by M.tb infection through in vitro cell experiments.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Hsa_circ_0001204 modulates inflammatory response of macrophages infected by Mycobacterium tuberculosis via TLR4/NF‐κB signalling pathway

Wang

Zhen

et al. 2022

Clin Exp Pharma Physio

View full text Add to dashboard Cite

Circular RNAs (circRNAs) play a vital role in the regulation of Mycobacterium tuberculosis (M.tb) by macrophages. In this project, the potential role of hsa_circ_0001204 in M.tb‐infected macrophages is explored. Hsa_circ_0001204 was determined in the patients with tuberculosis (TB) and M.tb‐infected macrophages. Its effect on the survival of M.tb and the apoptosis and inflammation of M.tb‐infected macrophages was evaluated. Toll‐like receptor 4/nuclear factor‐κB (TLR4/NF‐κB) signalling was detected by western blotting and immunofluorescence. TB patients and M.tb‐infected THP‐1 cells showed the significant downregulation of hsa_circ_0001204. Upregulating hsa_circ_0001204 reduced M.tb survival and suppressed the apoptosis and inflammatory response of THP‐1 cells. The TLR4/NF‐κB signalling pathway could be inhibited by hsa_circ_0001204 overexpression, which was activated by M.tb‐infection. Hsa_circ_0001204 confers protective effects in M.tb‐infected THP‐1 cells, at least partly via the inhibition of TLR4/NF‐κB signalling pathway.

show abstract

Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 85%

Section: Tuberculosis (Tb) Is a Deadly Infectious Disease Mainly Caus...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hsa_circ_0001204 modulates inflammatory response of macrophages infected by Mycobacterium tuberculosis via TLR4/NF‐κB signalling pathway

Wang

Zhen

et al. 2022

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…p38 is promoted by M. tuberculosis Rv2346c, a member of ESAT6, which induces the overexpression of miR-155 and miR-99b, leading to the inhibition of both the activation of NF-κB and secretion of cytokines including IL-6 and TNF-α, ultimately enhancing bacillary persistence and restraining the proliferation of BCG-infected macrophages ( 59 ). Targeting Rho-associated coiled-coil-forming protein kinase 1 (ROCK1), induction of miR-502-3p by M. tuberculosis decreases the production of TNF-α, IL-6, and IL-1β via the inhibition of the TLR4/NF-κB pathway, promoting pathogen survival ( 60 ).…”

Section: Immune Regulation Of Mirnas In Tuberculosismentioning

confidence: 99%

Immune regulation and emerging roles of noncoding RNAs in Mycobacterium tuberculosis infection

Liang

Ma²,

Gong³

et al. 2022

Front. Immunol.

View full text Add to dashboard Cite

Tuberculosis, caused by Mycobacterium tuberculosis, engenders an onerous burden on public hygiene. Congenital and adaptive immunity in the human body act as robust defenses against the pathogens. However, in coevolution with humans, this microbe has gained multiple lines of mechanisms to circumvent the immune response to sustain its intracellular persistence and long-term survival inside a host. Moreover, emerging evidence has revealed that this stealthy bacterium can alter the expression of demic noncoding RNAs (ncRNAs), leading to dysregulated biological processes subsequently, which may be the rationale behind the pathogenesis of tuberculosis. Meanwhile, the differential accumulation in clinical samples endows them with the capacity to be indicators in the time of tuberculosis suffering. In this article, we reviewed the nearest insights into the impact of ncRNAs during Mycobacterium tuberculosis infection as realized via immune response modulation and their potential as biomarkers for the diagnosis, drug resistance identification, treatment evaluation, and adverse drug reaction prediction of tuberculosis, aiming to inspire novel and precise therapy development to combat this pathogen in the future.

show abstract

The hsa_circ_0002371/hsa-miR-502-5p/ATG16L1 axis modulates the survival of intracellular Mycobacterium tuberculosis and autophagy in macrophages

Zhang,

He,

Ruan

et al. 2024

Cellular Signalling

View full text Add to dashboard Cite

MicroRNA‑502‑3p promotes Mycobacterium tuberculosis survival in macrophages by modulating the inflammatory response by targeting ROCK1

Cited by 6 publications

References 31 publications

Hsa_circ_0001204 modulates inflammatory response of macrophages infected by Mycobacterium tuberculosis via TLR4/NF‐κB signalling pathway

Hsa_circ_0001204 modulates inflammatory response of macrophages infected by Mycobacterium tuberculosis via TLR4/NF‐κB signalling pathway

Immune regulation and emerging roles of noncoding RNAs in Mycobacterium tuberculosis infection

The hsa_circ_0002371/hsa-miR-502-5p/ATG16L1 axis modulates the survival of intracellular Mycobacterium tuberculosis and autophagy in macrophages

Contact Info

Product

Resources

About