Mousazadeh Behzad, Sharebiani Hiva, Taheri Hossein, Valizedeh Narges, Fazeli Bahare
1Immunology Research Center, Inflammation and Inflammatory Diseases Division, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Surgery Department, Farabi Hospital, Mashhad, Iran.
Clin Mol Allergy. 2019 Jul 6;17:10. doi: 10.1186/s12948-019-0114-2. eCollection 2019.
The aim of this study was to determine if the inflammation of the sympathetic ganglia (SG) in thromboangiitis obliterans (TAO) is induced by an infectious pathogen inside or if it is a reactive sterile inflammation.
For the purpose of this study, the gene expression of high-mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), toll-like receptor 9 (TLR9), and the receptor for advanced glycation end-products (RAGE) were evaluated on the complementary DNA (cDNA) of the SG tissues of 24 TAO patients and two controls with hyperhidrosis by real-time polymerase chain reaction (PCR) and analysed by the Pfaffl method.
The gene expression of HMGB1 and TLR9 increased by about 25- and 2-fold changes in the SG of the TAO patients, respectively. However, there was no change in the gene expression of TLR4 or RAGE.
It appears that the inflammation in the SG of TAO patients is more likely a sterile inflammation, and its trigger may be mitochondrial DNA (mtDNA). Cadmium in cigarettes could be responsible for the induction of mtDNA release to the cell cytoplasm. In addition, the high expression of HMGB1 may play a role in the pathogenesis of TAO and may be responsible for both clinical manifestation of the disease and the imaging findings. Moreover, HMGB1 may be a target for treatment protocols for TAO. Further studies are highly recommended.
本研究的目的是确定血栓闭塞性脉管炎(TAO)中交感神经节(SG)的炎症是由内部感染病原体引起的,还是一种反应性无菌性炎症。
为了本研究的目的,通过实时聚合酶链反应(PCR)对24例TAO患者和2例多汗症对照者的SG组织互补DNA(cDNA)上的高迁移率族蛋白B1(HMGB1)、Toll样受体4(TLR4)、Toll样受体9(TLR9)和晚期糖基化终产物受体(RAGE)的基因表达进行评估,并采用Pfaffl法进行分析。
TAO患者SG中HMGB1和TLR9的基因表达分别增加了约25倍和2倍。然而,TLR4或RAGE的基因表达没有变化。
TAO患者SG中的炎症似乎更可能是无菌性炎症,其触发因素可能是线粒体DNA(mtDNA)。香烟中的镉可能导致mtDNA释放到细胞质中。此外,HMGB1的高表达可能在TAO的发病机制中起作用,可能是该疾病临床表现和影像学表现的原因。此外,HMGB1可能是TAO治疗方案的靶点。强烈建议进一步研究。