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脊柱关节炎中的肠道炎症与微生物群

Gut inflammation and microbiome in spondyloarthritis.

作者信息

Kabeerdoss Jayakanthan, Sandhya Pulukool, Danda Debashish

机构信息

Department of Clinical Immunology and Rheumatology, Christian Medical College, Vellore, Tamil Nadu, 632004, India.

出版信息

Rheumatol Int. 2016 Apr;36(4):457-68. doi: 10.1007/s00296-015-3414-y. Epub 2015 Dec 30.

Abstract

Spondyloarthritis (SpA) is chronic inflammatory disease involving joints and the spine. Bowel inflammation is common in SpA, which may be classified as acute or chronic. Chronic gut inflammation is most common in SpA patients with axial involvement as compared to those presenting with peripheral involvement alone. The pathogenesis of gut inflammation in SpA could be explained by two factors-over-activation of immunological cells and altered gut microbiome. This is exemplified by SpA animal models, namely HLA-B27-expressing transgenic animals and SKG mice models. Immunological mechanisms include homing of activated T cells from gut into synovium, excess pro-inflammatory cytokines secretion by immune cells such as IL-23 and genetic variations in immunological genes. The evidence for role of gut microbiome in SpA is gradually emerging. Recently, metagenomic study of gut microbiome by sequencing of microbial nucleic acids has enabled identification of new microbial taxa and their functions in gut of patients with SpA. In SpA, the gut microbiome could emerge as diagnostic and prognostic marker of disease. Modulation of gut microbiome is slated to have therapeutic potential as well.

摘要

脊柱关节炎(SpA)是一种累及关节和脊柱的慢性炎症性疾病。肠道炎症在SpA中很常见,可分为急性或慢性。与仅表现为外周受累的患者相比,慢性肠道炎症在有轴向受累的SpA患者中最为常见。SpA中肠道炎症的发病机制可由两个因素来解释——免疫细胞过度激活和肠道微生物群改变。这在SpA动物模型中得到了体现,即表达HLA - B27的转基因动物和SKG小鼠模型。免疫机制包括活化的T细胞从肠道归巢至滑膜、免疫细胞(如IL - 23)分泌过多促炎细胞因子以及免疫基因的遗传变异。肠道微生物群在SpA中的作用证据正在逐渐显现。最近,通过对微生物核酸进行测序的肠道微生物群宏基因组研究,已能够识别SpA患者肠道中的新微生物分类群及其功能。在SpA中,肠道微生物群可能成为疾病的诊断和预后标志物。调节肠道微生物群也有望具有治疗潜力。

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