Arthritis is the most common extra-intestinal complication in inflammatory bowel disease (IBD). Conversely, arthritis patients are at risk for developing IBD and often display subclinical gut inflammation. These observations suggest a shared disease etiology, commonly termed “the gut-joint-axis.” The clinical association between gut and joint inflammation is further supported by the success of common therapeutic strategies and microbiota dysbiosis in both conditions. Most data, however, support a correlative relationship between gut and joint inflammation, while causative evidence is lacking. Using two independent transgenic mouse arthritis models, either TNF- or IL-1β dependent, we demonstrate that arthritis develops independently of the microbiota and intestinal inflammation, since both lines develop full-blown articular inflammation under germ-free conditions. In contrast, TNF-driven gut inflammation is fully rescued in germ-free conditions, indicating that the microbiota is driving TNF-induced gut inflammation. Together, our study demonstrates that although common inflammatory pathways may drive both gut and joint inflammation, the molecular triggers initiating such pathways are distinct in these tissues.

中文翻译：

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无菌触发因素导致 TNF 和 IL-1β 依赖性小鼠关节炎模型中的关节炎症

关节炎是炎症性肠病（IBD）最常见的肠外并发症。相反，关节炎患者有患 IBD 的风险，并且经常表现出亚临床肠道炎症。这些观察结果表明存在共同的疾病病因，通常称为“肠道关节轴”。常见治疗策略的成功和这两种情况下微生物群的失调进一步支持了肠道和关节炎症之间的临床关联。然而，大多数数据支持肠道炎症和关节炎症之间存在相关性，但缺乏因果证据。使用两个独立的转基因小鼠关节炎模型（TNF-或IL-1β依赖性），我们证明关节炎的发展独立于微生物群和肠道炎症，因为这两个品系在无菌条件下都会产生全面的关节炎症。相比之下，TNF 驱动的肠道炎症在无菌条件下得到完全缓解，这表明微生物群正在驱动 TNF 诱导的肠道炎症。总之，我们的研究表明，尽管常见的炎症途径可能会导致肠道和关节炎症，但在这些组织中启动此类途径的分子触发因素是不同的。