Toll like receptor (TLR)-induced differential expression of microRNAs (MiRs) and immune response against infection: A systematic review

Aalaei‐Andabili, Seyed Hossein; Rezaei, Nima

doi:10.1016/j.jinf.2013.07.016

Cited by 31 publications

(17 citation statements)

References 112 publications

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“…4, C and D, caffeic acid phenethyl ester (CAPE)). There is another conceptually novel report identifying some microRNAs as negative regulators for LPS-dependent target genes (28,29). Among these microRNAs, miR1224 is likely a key inhibitor of Sp1 mRNA expression (29).…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

Ueno-Shuto

Kato

Tasaki

et al. 2014

Journal of Biological Chemistry

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Background: Single immunoglobulin interleukin-1 receptor-related molecule (SIGIRR) is a negative inflammatory regulator whose regulatory mechanism is mainly described in epithelial tissues. Results: Higher monocytic and neutrophilic SIGIRR expression is maintained by Sp1. Conclusion: Lipopolysaccharide decreases SIGIRR expression by suppressing Sp1 via the TLR4-p38 pathway. Significance: The LPS-dependent SIGIRR down-regulation may be critical for optimal inflammatory responses in immune cells.

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Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

Ueno-Shuto

Kato

Tasaki

et al. 2014

Journal of Biological Chemistry

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“…MiRNAs are single-stranded non-coding RNA molecules (containing roughly 22 nucleotides) that function in transcriptional and post-transcriptional gene regulation, by forming imperfect base pairs (13). MiRNAs have emerged as important controllers of many cellular events, including TLR signaling (14). MicroRNAs have also been shown as an important link between the innate and adaptive immune systems, potentially playing a role in the pathogenesis of inflammatory diseases (15-19).…”

Section: Introductionmentioning

confidence: 99%

miR-15a/16 Regulates Macrophage Phagocytosis after Bacterial Infection

Moon

Yang

Zheng

et al. 2014

The Journal of Immunology

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Bacterial infection and its associated sepsis are devastating clinical entities which lead to high mortality and morbidity in critically ill patients. Phagocytosis, along with other innate immune responses, exerts crucial impacts on the outcomes of these patients. MicroRNAs (miRNAs) are a novel class of regulatory noncoding RNAs targeting specific mRNAs for modulation of translation and expression of a targeted protein. The roles of miRNAs in host defense against bacterial sepsis remain unclear. We found that bacterial infections and/or bacterial-derived LPS enhanced the level of miR-15a/16 in bone marrow derived macrophages (BMDMs). Deletion of miR-15a/16 (miR-15a/16-/-) in myeloid cells significantly decreased the bacterial infection associated mortality in sepsis mouse models. Moreover, miR-15a/16 deficiency (miR-15a/16-/-) resulted in augmented phagocytosis and generation of mitochondrial reactive oxygen species (ROS) in BMDMs. Supportively, over-expression of miR-15a/16 using miRNA mimics led to decreased phagocytosis and decreased generation of mitochondrial ROS. Mechanistically, deletion of miR-15a/16 up-regulated the expression of toll-like receptor 4 (TLR4) via targeting the principle transcriptional regulator PU.1 locating on the promoter region of TLR4, and further modulated TLR4's downstream signaling molecules, including Rho GTPase Cdc 42 and TRAF6. Additionally, deficiency of miR-15a/16 also facilitated TLR4-mediated pro-inflammatory cytokine/chemokine release from BMDMs at the initial phase of infections. Taken together, miR-15a/16 altered phagocytosis and bacterial clearance by targeting, at least partially, on the TLR4-associated pathways, subsequently affecting the survival of septic mice.

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“…As shown in Fig. 1, microRNA-146a (miR-146a) is also involved in the host immune response to MTB infection by acting as a negative feedback regulator of the TLR/NF-kB pathway and potentially participating in regulating IL-17 expression by targeting the 3′-untranslated region (UTR) of the TRAF6 and the IRAK-1 genes1213. The activation of innate immunity receptors via a pathogen induces the up-regulation of miR-146a expression and will in turn exert a negative feedback on TLR4, leading to an inhibition of Th17 pathway molecules and pro-inflammatory cytokines (IL-17A, IL-17F, IL-6 and TNF-α) and an attenuation of the inflammatory effect of Th17 cells12.…”

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confidence: 99%

Genetic polymorphisms of IL-17A, IL-17F, TLR4 and miR-146a in association with the risk of pulmonary tuberculosis

Wang

et al. 2016

Sci Rep

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Genetic factors affect host susceptibility to pathogens. In this population-based case control study, we explored the genetic polymorphisms of IL-17, TLR4 and miR-146a in association with pulmonary tuberculosis in a Chinese Han population. We recruited 1601 pulmonary tuberculosis patients matched with 1526 healthy controls and genotyped twelve functional single nucleotide polymorphisms (SNPs). After the correction for multiple comparisons, two SNPs (rs10759932 and rs2737190) in the TLR4 gene remained significant. Individuals carrying the rs2737190-AG genotype (vs. AA) had a significantly increased risk of either clinical tuberculosis (OR: 1.31, 95% CI: 1.11–1.53) or sputum smear-positive tuberculosis (OR: 1.35, 95% CI: 1.13–1.61). Stratification analysis revealed that the effects of genetic variations on tuberculosis were more evident among non-smokers. People with haplotype TLR4 rs10983755G–rs10759932C had a significantly increased risk of tuberculosis (OR: 3.43, 95% CI: 2.34–5.05). Moreover, we found that SNPs of rs3819024 in IL-17A and rs763780 in IL-17F were weakly related to a prognosis of tuberculosis. Our results suggest that genetic polymorphisms of IL-17 and TLR4 may play a role in host susceptibility to tuberculosis in the Chinese Han population. More work is necessary to identify specific causative variants of tuberculosis underlying the observed associations.

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Toll like receptor (TLR)-induced differential expression of microRNAs (MiRs) and immune response against infection: A systematic review

Cited by 31 publications

References 112 publications

Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

miR-15a/16 Regulates Macrophage Phagocytosis after Bacterial Infection

Genetic polymorphisms of IL-17A, IL-17F, TLR4 and miR-146a in association with the risk of pulmonary tuberculosis

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