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Related Concept Videos

Chronic Bowel Disorders: Introduction01:17

Chronic Bowel Disorders: Introduction

Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
Irritable Bowel Syndrome (IBS) is a common disorder affecting the gastrointestinal tract. The distinctive feature is recurrent abdominal pain associated with altered bowel movements, manifesting as constipation, diarrhea, or fluctuating between both. The...
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Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

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 (Humira),...
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

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Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
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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...
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Inflammatory Bowel Disease IV: Clinical Manifestations

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Related Experiment Video

Updated: May 11, 2026

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease
05:08

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Published on: March 1, 2022

IgM turnover in Crohn's disease.

K B Jensen, N Goltermann, S Jarnum

    Gut
    |March 1, 1970
    PubMed
    Summary

    This study on Crohn's disease patients found increased IgM catabolism, correlating with serum levels. Researchers also observed linked synthesis rates for IgM and IgG, unaffected by protein loss.

    Area of Science:

    • Immunology
    • Gastroenterology
    • Biochemistry

    Background:

    • Crohn's disease is a chronic inflammatory condition affecting the gastrointestinal tract.
    • Immunoglobulin (Ig) metabolism alterations may play a role in Crohn's disease pathogenesis.
    • Previous studies have not fully elucidated the dynamics of IgM and IgG turnover in this patient population.

    Purpose of the Study:

    • To investigate the catabolic and synthetic rates of immunoglobulin M (IgM) and immunoglobulin G (IgG) in patients with Crohn's disease.
    • To assess the relationship between Ig turnover, serum Ig levels, and intestinal protein loss.
    • To explore correlations between IgM and IgG metabolism and disease activity or complications.

    Main Methods:

    • Simultaneous radioiodine-labeled IgM and IgG turnover studies were conducted in 12 Crohn's disease patients.

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    Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
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  • Intestinal protein loss was quantified using 59Fe-labeled iron dextran.
  • Serum immunoglobulin levels and fecal radioactivity were analyzed.

    • Main Results:

    • Elevated IgM catabolic rates were observed in most patients, positively correlating with serum IgM concentrations.
    • IgM and IgG synthetic rates showed a strong positive correlation.
    • Intestinal protein loss did not correlate with increased IgM or IgG catabolism, and fecal excretion of labeled Ig did not pinpoint lesion sites.

    Conclusions:

    • Increased IgM catabolism is a significant finding in Crohn's disease, linked to serum levels.
    • Coordinated synthesis of IgM and IgG suggests a systemic immune response.
    • Standard protein loss markers and fecal Ig excretion are insufficient to fully explain Ig metabolism disturbances in Crohn's disease.