Sterile triggers drive joint inflammation in TNF‐ and IL‐1β‐dependent mouse arthritis models

Author:

Thiran Alexandra123ORCID,Petta Ioanna123ORCID,Blancke Gillian123ORCID,Thorp Marie123ORCID,Planckaert Guillaume12ORCID,Jans Maude1234ORCID,Andries Vanessa123ORCID,Barbry Korneel2,Gilis Elisabeth12ORCID,Coudenys Julie12,Hochepied Tino24ORCID,Vanhove Christian5ORCID,Gracey Eric12ORCID,Dumas Emilie12ORCID,Manuelo Teddy12,Josipovic Ivan6,van Loo Geert234ORCID,Elewaut Dirk123ORCID,Vereecke Lars123ORCID

Affiliation:

1. Department of Internal Medicine and Pediatrics Ghent University Ghent Belgium

2. VIB‐UGent Center for Inflammation Research Ghent Belgium

3. Ghent Gut Inflammation Group (GGIG) Ghent Belgium

4. Department of Biomedical Molecular Biology Ghent University Ghent Belgium

5. Department of Electronics and Information Systems Ghent University, Faculty of Engineering & Architecture Ghent Belgium

6. Department of Physics and Astronomy – Radiation Physics, Faculty of Science, RP‐UGCT Ghent University Ghent Belgium

Abstract

AbstractArthritis 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.

Funder

Fonds Wetenschappelijk Onderzoek

Foundation for Research in Rheumatology

Bijzonder Onderzoeksfonds UGent

Publisher

Springer Science and Business Media LLC

Subject

Molecular Medicine

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