Inflammasomes contributing to inflammation in arthritis

Abstract

Inflammasomes are intracellular multiprotein signaling platforms that initiate inflammatory responses in response to pathogens and cellular damage. Active inflammasomes induce the enzymatic activity of caspase‐1, resulting in the induction of inflammatory cell death, pyroptosis, and the maturation and secretion of inflammatory cytokines IL‐1β and IL‐18. Inflammasomes are activated in many inflammatory diseases, including autoinflammatory disorders and arthritis, and inflammasome‐specific therapies are under development for the treatment of inflammatory conditions. In this review, we outline the different inflammasome platforms and recent findings contributing to our knowledge about inflammasome biology in health and disease. In particular, we discuss the role of the inflammasome in the pathogenesis of arthritic diseases, including rheumatoid arthritis, gout, ankylosing spondylitis, and juvenile idiopathic arthritis, and the potential of newly developed therapies that specifically target the inflammasome or its products for the treatment of inflammatory diseases.

Plant-Derived Nanovesicles: A Novel Form of Nanomedicine

“…Another way to modulate the innate immune response is to regulate the activation of particular inflammasomes ( Broz and Dixit, 2016 ; Ding et al, 2019 ; Spel and Martinon, 2020 ). Among various types of inflammasomes, nucleotide-binding domain and leucine-rich-repeat-containing family and pyrin domain-containing 3 (NLRP3) is implicated in Alzheimer’s disease and type 2 diabetes upon aberrant activation.…”

Associations Between the NLRP3 and IL-1β Gene Polymorphisms and Gout Susceptibility

“…IL-1β is a kind of pro-in ammatory cytokines,to a certain extent,production and release of IL-1β can resistance infection,but at the same time,there are correlations with gout,rheumatoid arthritis,chronic kidney disease,atherosclerosis and so on [27][28] .Studies have demonstrated that [29] IL-1β can promote the recruitment of neutrophil in the part of in ammation so that cause gout.In addition,IL-1β can make the person produces strong pain by activation injured receptor which exist in peripheral sensory nerve system sensitively and directly.The processing and secretion of IL-1β not only can through NOD-like receptor signaling pathways,but also can by Toll-like receptor signaling pathways.When MSU crystals are identi ed by Toll-like receptor,TLRs are able to interact with MyD88,make the MyD88 activation,leading to the activation of nuclear factor kappa B (NF-κB) and enter the nucleus to produce IL-1β,cause in ammation eventually through the cascade ampli cation effect [30][31] .…”

SARS-CoV-2 Inflammatory Syndrome. Clinical Features and Rationale for Immunological Treatment

“…Thus, it resembles the inflammatory syndromes that may complicate anti-phospholipid antibody syndrome (APS), namely the catastrophic anti-phospholipid syndrome (CAPs), characterized by disseminated intravascular microthrombosis [29]; or, the systemic CLLS characterized by altered capillary wall permeability [30]. Besides CAPs and CLLS, the SARS-CoV-2 inflammation, leading to ARDS, shares pathogenic mechanisms and clinical-radiological aspects with other auto-immune/-inflammatory diseases, such as juvenile idiopathic arthritis and its adult form [31][32][33] and Kawasaki disease [34]. Systemic CLLS has also been observed in Kawasaki disease [35].…”