Sterile triggers drive joint inflammation in TNF and IL-1beta dependent mouse arthritis models
Thiran, A.; Petta, I.; Blancke, G.; Thorp, M.; Plankaert, G.; Jans, M.; Andries, V.; Barbry, K.; Hochepied, T.; Vanhove, C.; Gracey, E.; Dumas, E.; Manuelo, T.; Josipovic, I.; van Loo, G.; Elewaut, D.; Vereecke, L.
Show abstract
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 & joint inflammation, while causative evidence is lacking. Using two independent transgenic mouse arthritis models, either TNF or IL1{beta} 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.
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