Abstract
The NOD LRR pyrin domain containing protein 3 (NLRP3) inflammasome is a cytosolic multi-proteins conglomerate with intrinsic ATPase activity. Their predominant presence in the immune cells emphasizes its significant role in immune response. The downstream effector proteins IL-1β and IL-18 are responsible for the biological functions of the NLRP3 inflammasome upon encountering the alarmins and microbial ligands. Although the NLRP3 inflammasome is essential for host defense during infections, uncontrolled activation and overproduction of IL-1β and IL-18 increase the risk of developing autoimmune and metabolic disorders. Emerging evidences suggest the action of lncRNAs in regulating the activity of NLRP3 inflammasome in various disease conditions. The long non-coding RNA (lncRNA) is an emerging field of study and evidence on their regulatory role in various diseases is grabbing attention. Recent studies emphasize the functions of lncRNAs in the fine control of the NLRP3 inflammasome at nuclear and cytoplasmic levels by interfering in chromatin architecture, gene transcription and translation. Recently, lncRNAs are also found to control the activity of various regulators of NLRP3 inflammasome. Understanding the precise role of lncRNA in controlling the activity of NLRP3 inflammasome helps us to design targeted therapies for multiple inflammatory diseases. The present review is a novel attempt to consolidate the substantial role of lncRNAs in the regulation of the NLRP3 inflammasome. A deeper insight on the NLRP3 inflammasome regulation by lncRNAs will help in developing targeted and beneficial therapeutics in the future.
Highlights
NOD LRR pyrin domain containing protein 3 (NLRP3) InflammasomeThe inflammasomes are a critical component of the innate immune system [1]
Activation of the NLRP3 inflammasome triggers pyroptosis, a caspase-1 dependent cell death, forces intracellular pathogens out of their replicative niche to the surroundings [4]. The exposure of such pathogens triggers further cytokine release from other immune cells leading to the generation of DAMPs that stimulate the immune cells to respond to the infection
Keeping in view the emerging affirmation about the critical role played by long non-coding RNA (lncRNA) in immune responses, in this review, we try to explore the involvement of lncRNA in regulating the activation and suppression of the NLRP3 inflammasome
Summary
The inflammasomes are a critical component of the innate immune system [1]. They are multimeric intracellular protein complexes that comprises a sensor protein termed pattern recognition receptor (PRR) that oligomerizes and forms a platform to activate the pro-caspase-1 in response to the damage associated and pathogen associated molecular patterns (DAMPs and PAMPs) [2]. Keeping in view the emerging affirmation about the critical role played by lncRNAs in immune responses, in this review, we try to explore the involvement of lncRNA in regulating the activation and suppression of the NLRP3 inflammasome. Zhang et al reported that lncRNA NEAT-1 (nuclear enriched abundant transcript 1) positively regulated the NLRP3 inflammasome assembly and cytokine production. LincRNA COX-2 assisted in enhancing the transcription of inflammatory genes by promoting the nuclear translocation of NF-κB p65 The translocation of these transcription factors into the nucleus led to the expression of NLRP3 inflammasome associated proteins [66]. ANRIL positively regulated the activation of NLRP3 inflammasome in UAN conditions by promoting the expression of BRCC3 [76]. The study showed that miR-223 overexpression suppressed the pyroptosis of HAECs and the effect of miR-223 on pyroptosis was reversed by the overexpression of lncRNA MEG3 [84]
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