Szabo Gyongyi, Iracheta-Vellve Arvin
University of Massachusetts Medical School, Department of Medicine, LRB 215, 364, Plantation Street, 01605 Worcester, United States.
University of Massachusetts Medical School, Department of Medicine, LRB 215, 364, Plantation Street, 01605 Worcester, United States.
Clin Res Hepatol Gastroenterol. 2015 Sep;39 Suppl 1:S18-23. doi: 10.1016/j.clinre.2015.06.012. Epub 2015 Jul 26.
Upregulation of the inflammatory cascade is a major element both in the progression of steatohepatitis to severe alcoholic hepatitis as well as in the progression of NASH to advanced NASH with fibrosis. The mechanisms underpinning these changes are only partially understood. Activation of the inflammatory cascade requires multiple stimuli and in this report, we discuss the role of inflammasomes that activate IL-1β as well as the sterile and pathogen-derived danger signals that results in inflammasome activation and inflammation in alcoholic and non-alcoholic steatohepatitis. The dynamics of inflammasome activation, the cell types involved and the trigger signals appear to be somewhat different between ASH and NASH. Further studies are needed to dissect the pathology-related differences between these two major forms of steatohepatitis. Clinical and therapeutic implications of inflammasome activation in steatohepatitis are also discussed.
炎症级联反应的上调是脂肪性肝炎进展为严重酒精性肝炎以及非酒精性脂肪性肝炎（NASH）进展为伴有纤维化的晚期NASH的主要因素。这些变化背后的机制仅得到部分理解。炎症级联反应的激活需要多种刺激，在本报告中，我们讨论了激活白细胞介素-1β的炎性小体的作用，以及导致炎性小体激活和酒精性及非酒精性脂肪性肝炎炎症的无菌和病原体衍生的危险信号。炎性小体激活的动态过程、涉及的细胞类型和触发信号在酒精性脂肪性肝炎（ASH）和NASH之间似乎有所不同。需要进一步研究剖析这两种主要形式的脂肪性肝炎之间与病理相关的差异。还讨论了炎性小体激活在脂肪性肝炎中的临床和治疗意义。
