MicroRNA-155: Regulation of Immune Cells in Sepsis

Abstract

MicroRNAs are small noncoding RNAs which regulate gene expression at the posttranscriptional level. miR-155 is encoded by the miR-155 host gene (miR155HG), also known as the noncoding B cell integration cluster (BIC). MicroRNAs are widely expressed in various hematopoietic cells and are involved in regulating the immune system. In this review, we summarized how miR-155 modulates specific immune cells and the regulatory role of miR-155 in sepsis. miR-155 is expressed by different populations of innate and adaptive immune cells and is involved in the regulation of development, proliferation, and function in these cells. Sepsis is associated with uncontrollable inflammatory responses, accompanied by unacceptably high mortality. Due to the inadequacy of diagnostic markers as well as treatment strategies, treating sepsis can be a huge challenge. So far, a large number of experiments have shown that the expression of miR-155 is increased at an early stage of sepsis and that this increase is positively correlated with disease progression and severity. In addition, by blocking the proinflammatory effects of miR-155, it can effectively improve sepsis-related organ injury, providing novel insights to identify potential biomarkers and therapeutic targets for sepsis. However, since most of the current research is limited to animal experiments, further clinical research is required to determine the function of miR-155 and its mechanism related to sepsis.

Human endothelial cell-derived exosomal microRNA-99a/b drives a sustained inflammatory response during sepsis by inhibiting mTOR expression

“…Although a number of exosomal miRNAs have been identified in sepsis, the functional effect of these dysregulated miRNA’s has not yet been fully elucidated. Exosomal miR-155 and miR-19b have both been shown to be increased during sepsis ( Alexander et al., 2015 ; Lv et al., 2020 ; Chen et al., 2021 ). Both of these miR’s induce the secretion of proinflammatory cytokines, including IL-6 and TNFα, by activating Nuclear Factor-κB (NF-ĸB) or through suppressor of cytokine signalling-1 (SOCS-1) ( Gantier et al., 2012 ; Yang et al., 2015 ; Ye et al., 2016 ; Mann et al., 2018 ).…”

Combinatorial microRNA Loading into Extracellular Vesicles for Increased Anti-Inflammatory Efficacy

“…HEK293T EVs were chosen for study due to their expected limited anti-inflammatory bioactivity as well as low intrinsic RNA content [ 29 ]. EVs were loaded with three different miRNA mimics (miR-146a, miR-155, and miR-223) that were found in the literature to be downregulated in septic patients, to regulate the TLR4 inflammatory pathway, and/or to have altered expression levels in response to LPS stimulation [ 4 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 ]. While certain single-stranded miRNAs (including miR-146a-5p) have been shown to be proinflammatory TLR agonists [ 3 , 9 , 39 , 40 ], these double-stranded mimics are designed to interact with the RNA-induced silencing complex (RISC) with preferential strand selection.…”

A Systematic Review of miRNA and cfDNA as Potential Biomarkers for Liquid Biopsy in Myocarditis and Inflammatory Dilated Cardiomyopathy

“…It is expressed in activated T cells, B cells, monocytes, and macrophages [ 23 ]. MiR-155 takes part in the immune response by promoting inflammation through the proliferation of macrophages, NK cells, and B and T cells, stimulating IL-6, TNF-alpha, and IFN-gamma synthesis, and other proinflammatory processes [ 24 ]. Corsten et al proved that in MCI miR-155 expression in heart tissue is localized mainly in macrophages and T cells [ 14 ].…”