[Neutrophils and selected cytokines in ulcerative colitis pathomechanism]

Krystyna Grzybowska1, Anna Kisiel, Ewa Fornalczyk-Wachowska

  • 1Klinika Pediatrii i Immunologii Wieku Rozwojowego UM w Lodzi.

Insights

Neutrophil markers CD11b and CD62L, along with inflammatory cytokines interleukin-1beta (IL-1beta), IL-6, and IL-8, are altered in children with ulcerative colitis (UC). These changes normalize during remission, indicating their role in disease activity.

Area of Science:

  • Pediatric Gastroenterology
  • Immunology
  • Hematology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease affecting children.
  • Neutrophil activation and inflammatory cytokine profiles are implicated in UC pathogenesis.
  • Understanding these markers in pediatric UC is crucial for assessing disease activity.

Purpose of the Study:

  • To evaluate the expression of CD11b and CD62L on neutrophils.
  • To measure serum levels of IL-1beta, IL-6, and IL-8.
  • To correlate these markers with disease severity and remission in pediatric UC.

Main Methods:

  • Assessed CD11b and CD62L expression on neutrophils in 30 children with UC.
  • Measured serum levels of IL-1beta, IL-6, and IL-8.
  • Compared findings during acute phase and remission with a control group of 12 children.

Main Results:

  • Elevated IL-1beta, IL-6, IL-8 serum levels and increased CD11b expression were observed in moderate to severe UC.
  • CD62L expression was significantly lower in UC patients compared to controls.
  • These changes normalized during remission, with IL-1beta elevation only in severe cases.

Conclusions:

  • Neutrophil priming and elevated pro-inflammatory cytokines are characteristic of active pediatric UC, particularly in severe cases.
  • CD11b and CD62L expression patterns, along with cytokine levels, can serve as indicators of disease activity.
  • Monitoring these biomarkers may aid in managing pediatric ulcerative colitis.

Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...