Revisiting the gut–joint axis: links between gut inflammation and spondyloarthritis

被引:0
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作者
Eric Gracey
Lars Vereecke
Dermot McGovern
Mareike Fröhling
Georg Schett
Silvio Danese
Martine De Vos
Filip Van den Bosch
Dirk Elewaut
机构
[1] VIB Center for Inflammation Research,Department of Internal Medicine and Pediatrics
[2] UZ Gent,Ghent Gut Inflammation Group
[3] Ghent University,F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute
[4] Ghent University,IBD Center, Department of Gastroenterology
[5] Cedars-Sinai Medical Center,Department of Biomedical Sciences
[6] Friedrich-Alexander University Erlangen-Nuremberg and Universitätsklinikum Erlangen,undefined
[7] Humanitas Clinical and Research Center – IRCCS –,undefined
[8] Rozzano,undefined
[9] Humanitas University,undefined
[10] Pieve Emanuele,undefined
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摘要
Gut inflammation is strongly associated with spondyloarthritis (SpA), as exemplified by the high prevalence of inflammatory bowel disease (IBD) and the even higher occurrence of subclinical gut inflammation in patients with SpA. The gut–joint axis of inflammation in SpA is further reinforced by similarities in immunopathogenesis at both anatomical sites and by the clinical success of therapies blocking TNF and IL-23 in IBD and in some forms of SpA. Many genetic risk factors are shared between SpA and IBD, and changes in the composition of gut microbiota are seen in both diseases. Current dogma is that inflammation in SpA initiates in the gut and leads to joint inflammation; however, although conceptually attractive, some research does not support this causal relationship. For example, therapies targeting IL-17A are efficacious in the joint but not the gut, and interfering with gut trafficking by targeting molecules such as α4β7 in IBD can lead to onset or flares of SpA. Several important knowledge gaps remain that must be addressed in future studies. Determining the true nature of the gut–joint axis has real-world implications for the treatment of patients with co-incident IBD and SpA and for the repurposing of therapeutics from one disease to the other.
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页码:415 / 433
页数:18
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