scholarly journals Monocytes from patients with rheumatoid arthritis and type 2 diabetes mellitus display an increased production of interleukin (IL)-1β via the nucleotide-binding domain and leucine-rich repeat containing family pyrin 3(NLRP3)-inflammasome activation: a pos

2015 ◽  
Vol 182 (1) ◽  
pp. 35-44 ◽  
Author(s):  
P. Ruscitti ◽  
P. Cipriani ◽  
P. Di Benedetto ◽  
V. Liakouli ◽  
O. Berardicurti ◽  
...  
2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Elisa Benetti ◽  
Fausto Chiazza ◽  
Nimesh S. A. Patel ◽  
Massimo Collino

The combination of obesity and type 2 diabetes is a serious health problem, which is projected to afflict 300 million people worldwide by 2020. Both clinical and translational laboratory studies have demonstrated that chronic inflammation is associated with obesity and obesity-related conditions such as insulin resistance. However, the precise etiopathogenetic mechanisms linking obesity to diabetes remain to be elucidated, and the pathways that mediate this phenomenon are not fully characterized. One of the most recently identified signaling pathways, whose activation seems to affect many metabolic disorders, is the “inflammasome,” a multiprotein complex composed of NLRP3 (nucleotide-binding domain and leucine-rich repeat protein 3), ASC (apoptosis-associated speck-like protein containing a CARD), and procaspase-1. NLRP3 inflammasome activation leads to the processing and secretion of the proinflammatory cytokines interleukin- (IL-) 1βand IL-18. The goal of this paper is to review new insights on the effects of the NLRP3 inflammasome activation in the complex mechanisms of crosstalk between different organs, for a better understanding of the role of chronic inflammation in metabolic disease pathogenesis. We will provide here a perspective on the current research on NLRP3 inflammasome, which may represent an innovative therapeutic target to reverse the detrimental metabolic consequences of the metabolic inflammation.


2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Adam H. Dyer ◽  
Isabella Batten ◽  
Conor Woods ◽  
James Gibney ◽  
Nollaig Bourke ◽  
...  

Author(s):  
Kirill V. Korneev ◽  
Ekaterina N. Sviriaeva ◽  
Nikita A. Mitkin ◽  
Alisa M. Gorbacheva ◽  
Aksinya N. Uvarova ◽  
...  

2019 ◽  
Vol 58 (10) ◽  
pp. 1383-1390 ◽  
Author(s):  
Hiroko Mori ◽  
Yosuke Okada ◽  
Mayuko Kawaguchi ◽  
Shigeru Iwata ◽  
Maiko Yoshikawa ◽  
...  

2020 ◽  
Vol 17 (6) ◽  
pp. 147916412097089
Author(s):  
Fotis Tsetsos ◽  
Athanasios Roumeliotis ◽  
Xanthippi Tsekmekidou ◽  
Sophia Alexouda ◽  
Stefanos Roumeliotis ◽  
...  

Background: Approximately one third of type 2 diabetes mellitus (T2DM) cases present with diabetic nephropathy (DN), the leading cause of end-stage renal disease. Inflammation plays an important role in T2DM disease and DN pathogenesis. NLRP3 inflammasomes are complexes that regulate interleukin-1B (IL-1B) and IL-18 secretion, both involved in inflammatory responses. Activation of NLRP3 is associated with DN onset and progression. Here, we explore whether DN is associated with variants in genes encoding key members of the NLRP3 inflammasome pathway. Methods: Using genome-wide association data, we performed a pilot case-control association study, between 101 DN-T2DM and 185 non-DN-T2DM cases from the Hellenic population across six NLRP3 inflammasome pathway genes. Results: Three common CARD8 variants confer decreased risk for DN, namely rs11665831 (OR = 0.62, p = 0.016), rs11083925 (OR = 0.65, p = 0.021), and rs2043211 (OR = 0.66, p = 0.026), independent of sex or co-inheritance with an IL-1B variant. Conclusion: CARD8 acts as an NLRP3, NF-κB and caspase-1 inhibitor; perhaps, alterations in the cross-talk between CARD8, NF-κB, and NLRP3, which could affect the pro-inflammatory environment in T2DM, render diabetic carriers of certain common CARD8 variants potentially less likely to develop T2DM-related pro-inflammatory responses followed by DN. These preliminary, yet novel, observations will require validation in larger cohorts from several ethnic groups.


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