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Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide...
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Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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Introduction
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Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
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IL-10 alleviates ulcerative colitis by regulating mitochondrial function through reducing ISG15 expression.

Zhi He1, Ya-Dong Feng2, Yue-Xin Zhang1

  • 1Center of Clinical Laboratory Medicine, Zhongda Hospital, Southeast University, 87 Ding Jiaqiao, Nanjing 210009, China.

Cellular Signalling
|June 20, 2025
PubMed
Summary

Interleukin-10 (IL-10) administration effectively treats ulcerative colitis (UC) by reducing inflammation and repairing the gut barrier. This cytokine therapy activates autophagy and modulates ISG15 expression, offering a promising therapeutic strategy for UC patients.

Keywords:
AutophagyIL-10ISG15Intestinal barrierMitochondrial functionUlcerative colitis

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Area of Science:

  • Gastroenterology
  • Immunology
  • Molecular Biology

Background:

  • Interleukin-10 (IL-10) is an anti-inflammatory cytokine with potential therapeutic applications in autoimmune diseases.
  • The specific effects of IL-10 on ulcerative colitis (UC) remain incompletely understood.
  • This research investigates IL-10's efficacy in suppressing UC flares.

Purpose of the Study:

  • To evaluate the therapeutic potential of Interleukin-10 (IL-10) in managing ulcerative colitis (UC).
  • To elucidate the molecular mechanisms underlying IL-10's effects on intestinal inflammation, apoptosis, and oxidative stress.

Main Methods:

  • Established a mouse model of UC using dextran sulfate sodium (DSS).
  • Utilized lipopolysaccharide (LPS)-stimulated Caco-2 cells to investigate molecular pathways.
  • Analyzed Interferon-Stimulated Gene 15 (ISG15) expression and autophagy markers (ATG7, LC3-II/LC3-I ratio).

Main Results:

  • IL-10 administration significantly improved clinical outcomes in DSS-induced colitis, including weight recovery and increased colon length.
  • IL-10 protected intestinal epithelial cells by inhibiting apoptosis, reducing pro-inflammatory cytokines, and modulating oxidative stress markers.
  • IL-10 enhanced autophagy, suppressed ISG15 upregulation, and reduced apoptosis and oxidative stress in Caco-2 cells; these effects were abrogated by autophagy inhibition or ISG15 overexpression.

Conclusions:

  • IL-10 administration effectively suppresses UC progression by activating autophagy and modulating ISG15.
  • Targeted delivery of IL-10 to the intestinal lamina propria could enhance therapeutic efficacy and minimize side effects.