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nicotine and NLRP3

Yang Yao, Junjun Mao, Shouzhu Xu, Lei Zhao, Lihui Long, Lin Chen, Dongmin Li, Shemin Lu
Atherosclerosis is widely known to be a chronic inflammatory disease. C-reactive protein (CRP), an important inflammatory factor, plays an essential role in the pathogenesis of atherosclerosis. Nicotine, the main addictive component of cigarette, has been shown to induce the production of CRP. The aim of this study was to investigate the effect of rosmarinic acid (RA), a polyphenol with antiinflammatory activity, on nicotine-induced elevation of CRP in vascular smooth muscle cells (VSMCs). We found that pretreatment of VSMCs with RA attenuated nicotine-induced expression of CRP in a time- and dose-dependant manner...
August 26, 2018: Journal of Cellular Physiology
Xianxian Wu, Haiying Zhang, Wei Qi, Ying Zhang, Jiamin Li, Zhange Li, Yuan Lin, Xue Bai, Xin Liu, Xiaohui Chen, Huan Yang, Chaoqian Xu, Yong Zhang, Baofeng Yang
Cigarette smoking is a major risk factor for atherosclerosis and other cardiovascular diseases. Increasing evidence has demonstrated that nicotine impairs the cardiovascular system by targeting vascular endothelial cells, but the underlying mechanisms remain obscure. It is known that cell death and inflammation are crucial processes leading to atherosclerosis. We proposed that pyroptosis may be implicated in nicotine-induced atherosclerosis and therefore conducted the present study. We found that nicotine resulted in larger atherosclerotic plaques and secretion of inflammatory cytokines in ApoE-/- mice fed with a high-fat diet (HFD)...
February 7, 2018: Cell Death & Disease
Ping Ke, Bo-Zong Shao, Zhe-Qi Xu, Xiong-Wen Chen, Wei Wei, Chong Liu
AIMS: To evaluate whether activating α7 nicotinic acetylcholine receptor (α7nAChR) could inhibit the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome through regulation of β-arrestin-1 in monocyte/macrophage system, thus contributing to the control of neuroinflammation. METHODS: The protein levels of NLRP3, caspase-1 (Casp-1) p20 and proCasp-1, interleukin-1β (IL-1β) p17 and proIL-1β, IL-18 and proIL-18 were measured using Western blotting...
November 2017: CNS Neuroscience & Therapeutics
Yanxiang Li, Guangde Yang, Xiaofeng Yang, Weirong Wang, Jiye Zhang, Yanhao He, Wei Zhang, Ting Jing, Rong Lin
Emerging evidences indicated that NLRP3 inflammasome initiates inflammatory response involved in cardiovascular disease. Nicotinic acid (NA) has been known to possess potential anti-inflammatory property. The aim of this study was to investigate the effect of NA on the activation of NLRP3 inflammasome and the underlying mechanisms. It was found that lipopolysaccharide (LPS) and adenosine triphosphate (ATP) triggered the activation of NLRP3 inflammasome in human umbilical vein endothelial cells (HUVECs). NA inhibited NLRP3 inflammasome activation and subsequent caspase-1 cleavage as well as interleukin (IL)-1β secretion...
November 2016: International Immunopharmacology
Andreas Hecker, Mira Küllmar, Sigrid Wilker, Katrin Richter, Anna Zakrzewicz, Srebrena Atanasova, Verena Mathes, Thomas Timm, Sabrina Lerner, Jochen Klein, Andreas Kaufmann, Stefan Bauer, Winfried Padberg, Wolfgang Kummer, Sabina Janciauskiene, Martin Fronius, Elke K H Schweda, Günter Lochnit, Veronika Grau
IL-1β is a potent proinflammatory cytokine of the innate immune system that is involved in host defense against infection. However, increased production of IL-1β plays a pathogenic role in various inflammatory diseases, such as rheumatoid arthritis, gout, sepsis, stroke, and transplant rejection. To prevent detrimental collateral damage, IL-1β release is tightly controlled and typically requires two consecutive danger signals. LPS from Gram-negative bacteria is a prototypical first signal inducing pro-IL-1β synthesis, whereas extracellular ATP is a typical second signal sensed by the ATP receptor P2X7 that triggers activation of the NLRP3-containing inflammasome, proteolytic cleavage of pro-IL-1β by caspase-1, and release of mature IL-1β...
September 1, 2015: Journal of Immunology: Official Journal of the American Association of Immunologists
Laurence Macia, Jian Tan, Angelica T Vieira, Katie Leach, Dragana Stanley, Suzanne Luong, Mikako Maruya, Craig Ian McKenzie, Atsushi Hijikata, Connie Wong, Lauren Binge, Alison N Thorburn, Nina Chevalier, Caroline Ang, Eliana Marino, Remy Robert, Stefan Offermanns, Mauro M Teixeira, Robert J Moore, Richard A Flavell, Sidonia Fagarasan, Charles R Mackay
Diet and the gut microbiota may underpin numerous human diseases. A major metabolic product of commensal bacteria are short-chain fatty acids (SCFAs) that derive from fermentation of dietary fibre. Here we show that diets deficient or low in fibre exacerbate colitis development, while very high intake of dietary fibre or the SCFA acetate protects against colitis. SCFAs binding to the 'metabolite-sensing' receptors GPR43 and GPR109A in non-haematopoietic cells mediate these protective effects. The inflammasome pathway has hitherto been reported as a principal pathway promoting gut epithelial integrity...
April 1, 2015: Nature Communications
Ben Lu, Kevin Kwan, Yaakov A Levine, Peder S Olofsson, Huan Yang, Jianhua Li, Sonia Joshi, Haichao Wang, Ulf Andersson, Sangeeta S Chavan, Kevin J Tracey
The mammalian immune system and the nervous system coevolved under the influence of cellular and environmental stress. Cellular stress is associated with changes in immunity and activation of the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome, a key component of innate immunity. Here we show that α7 nicotinic acetylcholine receptor (α7 nAchR)-signaling inhibits inflammasome activation and prevents release of mitochondrial DNA, an NLRP3 ligand. Cholinergic receptor agonists or vagus nerve stimulation significantly inhibits inflammasome activation, whereas genetic deletion of α7 nAchR significantly enhances inflammasome activation...
August 14, 2014: Molecular Medicine
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