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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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Risk Factors
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Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy01:30

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Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
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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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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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Inverse Relationship Between Clock Gene Expression and Inflammatory Markers in Ulcerative Colitis Patients Undergoing

Y Weintraub1,2, S Cohen2,3, A Anafy2,3

  • 1Institute of Gastroenterology, Nutrition and Liver Diseases, Schneider Children's Medical Center, Petach Tikva, Israel.

Digestive Diseases and Sciences
|February 6, 2023
PubMed
Summary
This summary is machine-generated.

Inflammatory bowel disease (IBD) patients show altered clock gene expression, which normalizes with reduced inflammation. This suggests clock gene dysregulation is linked to IBD activity and may be reversible.

Keywords:
CRPCircadian rhythmsClinical remissionClock gene expressionUC

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Area of Science:

  • Chronobiology
  • Gastroenterology
  • Molecular Biology

Background:

  • Clock gene expression is altered in patients with inflammatory bowel disease (IBD).
  • The relationship between inflammation levels and clock gene expression in IBD requires further investigation.

Purpose of the Study:

  • To determine if reduced inflammation in IBD patients restores clock gene expression to levels observed in healthy individuals.
  • To investigate the association between inflammatory markers and specific clock gene expression in IBD.

Main Methods:

  • A prospective study involving 49 IBD patients and 19 healthy controls.
  • Collected data on demographics, sleep, disease activity, C-reactive protein (CRP), and fecal calprotectin (Fcal).
  • Analyzed peripheral blood for clock gene (CLOCK, BMAL1, CRY1, CRY2, PER1, PER2) expression in ulcerative colitis (UC) and Crohn's disease (CD) patients, categorized by disease activity.

Main Results:

  • Reduced BMAL1 and PER2 expression in active UC patients compared to those in remission.
  • BMAL1, PER1, and PER2 levels were lower in UC patients with elevated CRP.
  • PER2, CRY1, and CRY2 were reduced in UC patients with high Fcal levels.
  • Clock gene expression in UC patients in remission was comparable to healthy controls.
  • An overshoot in CRY1 expression was noted in IBD patients in remission or with lower inflammatory markers.

Conclusions:

  • C-reactive protein (CRP) and fecal calprotectin (Fcal) show an inverse relationship with clock gene levels in ulcerative colitis (UC).
  • CRY1 may play a role in counter-regulating anti-inflammatory processes during IBD remission induction.