ArticleEMBO molecular medicine2023
Sterile triggers drive joint inflammation in TNF- and IL-1β-dependent mouse arthritis models.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- CARD14 signaling in intestinal epithelial cells induces intestinal inflammation and intestinal transit delay.EMBO molecular medicine · 2025Article
- Pyrin inflammasome-driven erosive arthritis caused by unprenylated RHO GTPase signaling.EMBO molecular medicine · 2025Article
- Anti-inflammatory effects of natural polysaccharides: molecular mechanisms and nanotherapeutic applications.Frontiers in immunology · 2025Review
- Myeloid A20 is critical for alternative macrophage polarization and type-2 immune-mediated helminth resistance.Frontiers in immunology · 2024Article
- Sterile triggers drive joint inflammation in TNF- and IL-1β-dependent mouse arthritis models.EMBO molecular medicine · 2023Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
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 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.
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Registered trials
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