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Decrease in systemic tolerance to fed ovalbumin in indomethacin-treated mice

E Louis1, D Franchimont, M Deprez

  • 1Department of Gastroenterology, CHU of Liège, Belgium.

International Archives of Allergy and Immunology
|January 1, 1996
PubMed
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Non-steroidal anti-inflammatory drugs (NSAID) increase intestinal permeability, allowing antigens to penetrate the gut. This NSAID effect reduces systemic tolerance to food antigens, potentially contributing to NSAID enteropathy.

Area of Science:

  • Gastroenterology
  • Immunology
  • Pharmacology

Background:

  • Oral non-steroidal anti-inflammatory drugs (NSAID) increase intestinal permeability and cause inflammatory lesions.
  • Mechanisms behind NSAID-induced inflammatory lesions are not fully understood.
  • Increased permeability may lead to abnormal immune responses to dietary antigens and bacterial products.

Purpose of the Study:

  • To investigate the impact of indomethacin on ovalbumin serum levels and systemic immune response in mice.
  • To explore the relationship between indomethacin dosage, antigen penetration, and immune tolerance.

Main Methods:

  • Mice were orally administered ovalbumin and varying doses of indomethacin.
  • Ovalbumin serum levels were measured.
  • Systemic humoral and cellular immune responses to ovalbumin were assessed.

Related Experiment Videos

  • Intestinal tissues were examined for lesions.

    • Main Results:

    • Indomethacin administration increased ovalbumin serum levels in a dose-dependent manner.
    • Increased ovalbumin levels correlated with epithelial and subepithelial intestinal lesions.
    • Systemic humoral and cellular tolerance to ovalbumin were partially abrogated in indomethacin-treated mice.

    Conclusions:

    • Oral indomethacin increases intestinal antigen passage and decreases systemic tolerance to luminal antigens in mice.
    • This decrease in tolerance may play a role in the development of NSAID enteropathy.
    • Potential contributing factors include epithelial barrier dysfunction and direct immunomodulatory effects of indomethacin.