Bioinformatics and Medical Informatics Research Center, San Diego State University, 5500 Campanile Dr., 92182 San Diego, CA USA.
Biomed Pharmacother. 2017 Aug;92:819-825. doi: 10.1016/j.biopha.2017.05.126. Epub 2017 Jun 6.
Inflammation is a pivotal defense system of body. Unfortunately, when homeostasis falters, the same inflammatory mechanism acts as a double-edged sword, and turns offensive, paving the path for a broad array of pathologies. A multi-protein complex termed as inflammasome perceives the PAMPs (pathogen associated molecular patterns) and DAMPs (danger associated molecular patterns), executing immune responses. This activation predominantly encompasses the elaboration of effector cytokines IL-1β, IL-18, and the cysteine proteases (caspase 1 and 11). Extensive study on an inflammasome NLRP3 has revealed its role in the onset and progression of pathogenic, metabolic, autoimmune, neural, and geriatric diseases. In this regard, this inflammasome's immune activation mechanisms and inhibition strategies have been discussed. Through this rigorous literature analysis, the superficial diversity between pathogens/allergens and mutagens, and NLRP3 activity towards them has been emphasized. Though there is a scope for inhibition of aberrant inflammasomes, including that of NLRP3, given their complexity and unpredictability, prevention of their activation by lifestyle correction has been suggested.
炎症是身体的关键防御系统。不幸的是，当体内平衡失调时，同样的炎症机制就像一把双刃剑，变得具有攻击性，为多种病理铺平了道路。一种称为炎性体的多蛋白复合物可以感知 PAMPs（病原体相关分子模式）和 DAMPs（危险相关分子模式），从而执行免疫反应。这种激活主要包括效应细胞因子 IL-1β、IL-18 和半胱氨酸蛋白酶（caspase 1 和 11）的产生。对炎性体 NLRP3 的广泛研究揭示了它在致病性、代谢性、自身免疫性、神经退行性和老年疾病的发病和进展中的作用。在这方面，讨论了这种炎性体的免疫激活机制和抑制策略。通过对文献的严格分析，强调了病原体/过敏原和诱变剂之间的表面差异，以及 NLRP3 对它们的活性。虽然有抑制异常炎性体的空间，包括 NLRP3，但鉴于它们的复杂性和不可预测性，建议通过生活方式的改变来预防它们的激活。
