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

Alexandra Thiran (UGent) , Ioanna Petta (UGent) , Gillian Blancke (UGent) , Marie Thorp (UGent) , Guillaume Planckaert (UGent) , Maude Jans (UGent) , Vanessa Andries (UGent) , Korneel Barbry (UGent) , Elisabeth Gilis (UGent) , Julie Coudenys (UGent) , et al.
(2023) EMBO MOLECULAR MEDICINE. 15(10).
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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-1b 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.
Keywords
Molecular Medicine, microbiome, intestinal inflammation, gut-joint axis, germ-free, arthritis

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MLA
Thiran, Alexandra, et al. “Sterile Triggers Drive Joint Inflammation in TNF‐ and IL-1β‐dependent Mouse Arthritis Models.” EMBO MOLECULAR MEDICINE, vol. 15, no. 10, 2023, doi:10.15252/emmm.202317691.
APA
Thiran, A., Petta, I., Blancke, G., Thorp, M., Planckaert, G., Jans, M., … Vereecke, L. (2023). Sterile triggers drive joint inflammation in TNF‐ and IL-1β‐dependent mouse arthritis models. EMBO MOLECULAR MEDICINE, 15(10). https://doi.org/10.15252/emmm.202317691
Chicago author-date
Thiran, Alexandra, Ioanna Petta, Gillian Blancke, Marie Thorp, Guillaume Planckaert, Maude Jans, Vanessa Andries, et al. 2023. “Sterile Triggers Drive Joint Inflammation in TNF‐ and IL-1β‐dependent Mouse Arthritis Models.” EMBO MOLECULAR MEDICINE 15 (10). https://doi.org/10.15252/emmm.202317691.
Chicago author-date (all authors)
Thiran, Alexandra, Ioanna Petta, Gillian Blancke, Marie Thorp, Guillaume Planckaert, Maude Jans, Vanessa Andries, Korneel Barbry, Elisabeth Gilis, Julie Coudenys, Tino Hochepied, Christian Vanhove, Eric Gracey, Emilie Dumas, Teddy Manuello, Iván Josipovic, Geert van Loo, Dirk Elewaut, and Lars Vereecke. 2023. “Sterile Triggers Drive Joint Inflammation in TNF‐ and IL-1β‐dependent Mouse Arthritis Models.” EMBO MOLECULAR MEDICINE 15 (10). doi:10.15252/emmm.202317691.
Vancouver
1.
Thiran A, Petta I, Blancke G, Thorp M, Planckaert G, Jans M, et al. Sterile triggers drive joint inflammation in TNF‐ and IL-1β‐dependent mouse arthritis models. EMBO MOLECULAR MEDICINE. 2023;15(10).
IEEE
[1]
A. Thiran et al., “Sterile triggers drive joint inflammation in TNF‐ and IL-1β‐dependent mouse arthritis models,” EMBO MOLECULAR MEDICINE, vol. 15, no. 10, 2023.
@article{01HA9JNTS9QXVKAD9WFYXW32VE,
  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-1b 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.}},
  articleno    = {{e17691}},
  author       = {{Thiran, Alexandra and Petta, Ioanna and Blancke, Gillian and Thorp, Marie and Planckaert, Guillaume and Jans, Maude and Andries, Vanessa and Barbry, Korneel and Gilis, Elisabeth and Coudenys, Julie and Hochepied, Tino and Vanhove, Christian and Gracey, Eric and Dumas, Emilie and Manuello, Teddy and Josipovic, Iván and van Loo, Geert and Elewaut, Dirk and Vereecke, Lars}},
  issn         = {{1757-4676}},
  journal      = {{EMBO MOLECULAR MEDICINE}},
  keywords     = {{Molecular Medicine,microbiome,intestinal inflammation,gut-joint axis,germ-free,arthritis}},
  language     = {{eng}},
  number       = {{10}},
  pages        = {{17}},
  title        = {{Sterile triggers drive joint inflammation in TNF‐ and IL-1β‐dependent mouse arthritis models}},
  url          = {{http://doi.org/10.15252/emmm.202317691}},
  volume       = {{15}},
  year         = {{2023}},
}
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