JAK/STAT signaling promotes the emergence of unique cell states in ulcerative colitis

Maciag, Grzegorz; Hansen, Stine Lind; Krizic, Kata; Kellermann, Lauge; Inventor Zøylner, Maureen Joy; Ulyanchenko, Svetlana; Maimets, Martti; Baattrup, Astrid Møller; Riis, Lene Buhl; Khodosevich, Konstantin; Sato, Toshiro; Bressan, Raul Bardini; Nielsen, Ole Haagen; Jensen, Kim B.

doi:10.1016/j.stemcr.2024.06.006

Stem Cell Reports

2024

DOI: 10.1016/j.stemcr.2024.06.006

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JAK/STAT signaling promotes the emergence of unique cell states in ulcerative colitis

Grzegorz Maciag,

Stine Lind Hansen,

Kata Krizic

et al.

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2024

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Tofacitinib and budesonide treatment affect stemness and chemokine release in IBD patient-derived colonoids

Srid,

Bakke,

Gopalakrishnan

et al. 2024

Preprint

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Restoration of the intestinal epithelial barrier is crucial for achieving mucosal healing, the therapeutic goal for inflammatory bowel diseases (IBD). During homeostasis, epithelial renewal is maintained by crypt stem cells and progenitors that cease to divide as they differentiate into mature colonocytes. Inflammation is a major effector of mucosal damage in IBD and has been found to affect epithelial stemness, regeneration and cellular functions. However, the impact of immune cell-modulating IBD drugs on epithelial homeostasis and repair is poorly understood. It is likely that these drugs will have distinct mechanisms of action (MOA) in intestinal epithelium relevant for homeostasis that will vary among patients. We investigated cellular effects of pan-Janus Kinase (JAK) inhibitor tofacitinib and the corticosteroid budesonide on uninflamed and TNF + Poly(I:C) stimulated human colon organoids (colonoids) from healthy donors and IBD-patients. Our findings reveal that although both tofacitinib and budesonide exhibit anti-inflammatory effects, tofacitinib increased colonoid size and proliferation during differentiation, and promoted epithelial stemness. In contrast, budesonide decreased colonoid size and showed no consistent effect on proliferation or stemness. Our study demonstrates the value of employing human colonoids to investigate how IBD drugs affect intestinal epithelial cells and inter-individual variations relevant to mucosal healing and personalized IBD treatment.

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Tofacitinib and budesonide treatment affect stemness and chemokine release in IBD patient-derived colonoids

Srid,

Bakke,

Gopalakrishnan

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

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JAK/STAT signaling promotes the emergence of unique cell states in ulcerative colitis

Cited by 1 publication

References 33 publications

Tofacitinib and budesonide treatment affect stemness and chemokine release in IBD patient-derived colonoids

Tofacitinib and budesonide treatment affect stemness and chemokine release in IBD patient-derived colonoids

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