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The gut-joint axis in spondyloarthritis: immunological, microbial, and clinical insights
Seminars in Immunopathology ( IF 7.9 ) Pub Date : 2021-02-24 , DOI: 10.1007/s00281-021-00845-0
Zoya Qaiyum 1 , Melissa Lim 1 , Robert D Inman 1, 2, 3
Affiliation  

The strong genetic and clinical overlaps between spondyloarthritis (SpA) and inflammatory bowel disease (IBD) have placed much needed focus on the gut-joint axis of inflammation in SpA, leading to three key hypotheses that attempt to unravel this complex relationship. The arthritogenic peptide hypothesis and the aberrant cellular trafficking hypothesis have been put forth to rationalize the manner by which the innate and adaptive immune systems cooperate and converge during SpA pathogenesis. The bacterial dysbiosis hypothesis discusses how changes in the microbiome lead to architectural and immunological consequences in SpA. These theories are not mutually exclusive, but can provide an explanation as to why subclinical gut inflammation may sometimes precede joint inflammation in SpA patients, thereby implying a causal relationship. Such investigations will be important in informing therapeutic decisions which may be common to both SpA and IBD. However, these hypotheses can also offer insights for a coincident inflammatory relationship between the gut and the joint, particularly when assessing the immunological players involved. Insights from understanding how these systems might affect the gut and joint differently will be equally imperative to address where the therapeutic differences lie between the two diseases. Collectively, this knowledge has practical implications in predicting the likelihood of IBD development in SpA or presence of coincident SpA-IBD, uncovering novel therapeutic targets, and redesigning currently approved treatments. It is evident that a multidisciplinary approach between the rheumatology and gastroenterology fields cannot be ignored, when it comes to the care of SpA patients at risk of IBD or vice versa.



中文翻译:

脊柱关节炎中的肠关节轴:免疫学、微生物学和临床见解

脊柱关节炎 (SpA) 和炎症性肠病 (IBD) 之间强烈的遗传和临床重叠使得 SpA 中炎症的肠-关节轴非常需要关注,导致三个关键假设试图解开这种复杂的关系。已经提出了关节炎肽假说和异常细胞运输假说,以合理化先天和适应性免疫系统在 SpA 发病过程中合作和收敛方式细菌失调假说讨论了微生物组的变化如何导致 SpA 的结构和免疫学后果。这些理论并不相互排斥,但可以解释为什么亚临床肠道炎症有时可能先于 SpA 患者的关节炎症,从而暗示因果关系。此类调查对于为 SpA 和 IBD 可能共有的治疗决策提供信息非常重要。然而,这些假设也可以为肠道和关节之间同时存在的炎症关系提供见解,特别是在评估所涉及的免疫学参与者时。了解这些系统如何以不同方式影响肠道和关节的见解对于解决两种疾病之间的治疗差异所在同样重要。集体,这一知识在预测 SpA 中 IBD 发展的可能性或同时存在 SpA-IBD、发现新的治疗靶点和重新设计当前批准的治疗方面具有实际意义。显然,对于有 IBD 风险的 SpA 患者的护理,风湿病学和胃肠病学领域之间的多学科方法不容忽视,反之亦然。

更新日期:2021-02-24
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