Can microRNAs keep inflammasomes in check?

Department of Internal Medicine, Division of Allergy and Immunology, Morsani College of Medicine, University of South Florida Tampa, FL, USA.
Frontiers in Genetics 03/2013; 4:30. DOI: 10.3389/fgene.2013.00030
Source: PubMed
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    • "It was recently reported that caspase-1-mediated processing of IL-1β is mediated by inflammasomes in various pathological conditions (Kolliputi et al., 2010, 2012; Fukumoto et al., 2013). Inflammasomes, such as the NLRP3 inflammasome, detect the inflammatory aggregates of β-amyloid and inactive IL- 1β, and respond by secreting caspase-1 (Casp-1) to activate IL-1β (Heneka et al., 2013; Qazi et al., 2013). This leads to the creation of an inflammatory environment around the plaque, which downregulates amyloid precursor protein (APP) degradation, as well as decreased destruction of β-amyloid plaques by microglia (Figure 1). "

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    ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is a manifestation of metabolic syndrome, a group of conditions including hypertension, high plasma glucose, excess body fat around waist or abnormal cholesterol levels which will work together to increase the risk of heart disease, diabetes, and stroke (Kim and Younossi, 2008). Although 20% of NAFLD cases progress to non-alcoholic steatohepatitis (NASH), the exact cause of the disease progression is uncertain (Lucy Bird, 2012; Ibrahim et al., 2013). Gut and liver are connected via the portal circulation and through embryogenesis they are clearly linked. Researchers hypothesized that due to this link, imbalances in the gut could influence liver disease. Normal gut flora plays a significant role in keeping our innate immune system intact and when dysbiosis occurs, it may lead to various inflammatory diseases (Wood, 2012). Inflammasomes are recently discovered multiprotein complexes involved in a diverse range of inflammatory pathologies (Kolliputi et al., 2010, 2012). A specific inflammasome sensor consists of nucleoside-triphosphatase domain (NACHT), leucine rich repeat (LRR), and pyrin domain (PYD), which are domains-containing protein 3 (NLRP3) (Lane et al., 2013; Qazi et al., 2013). Toll-like receptors (TLRs) are a different subset of "danger-sensing" receptors that trigger proinflammatory gene expression (Janssens and Beyaert, 2003). © 2013 Desai, Tamarapu Parthasarathy, Galam, Lockey and Kolliputi.
    Full-text · Article · Jul 2013 · Frontiers in Physiology

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