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T cell activation alters intestinal structure and function.

Michael Field1

  • 1Division of Digestive and Liver Diseases (emeritus), Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York, USA. mf9@columbia.edu

The Journal of Clinical Investigation
|October 4, 2006
PubMed
Summary
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Anti-CD3 antibody treatment causes diarrhea by altering jejunal epithelial permeability and inhibiting sodium absorption. Increased interstitial pressure, likely from TNF effects, drives fluid accumulation.

Area of Science:

  • Gastroenterology
  • Immunology
  • Physiology

Background:

  • Treatment with anti-CD3 antibody (anti-CD3) is known to induce transient diarrhea.
  • Tumor necrosis factor (TNF) is implicated in inflammatory conditions affecting the gastrointestinal tract.

Purpose of the Study:

  • To investigate the mechanisms by which anti-CD3 antibody and TNF induce fluid accumulation in the jejunum.
  • To elucidate the epithelial and non-epithelial cellular changes responsible for anti-CD3-induced diarrhea.

Main Methods:

  • Mice were injected with anti-CD3 antibody or TNF.
  • Jejunal tissues were analyzed for fluid accumulation, epithelial cell phenotype changes, protein and solute permeability, and brush border Na+/H+ exchanger activity.
  • The role of cytokine LIGHT was also assessed.

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Main Results:

  • Anti-CD3 and TNF induced fluid accumulation and altered jejunal epithelial phenotype.
  • Epithelial changes included increased passive permeability to proteins, solutes, and water, and endocytosis of the Na+/H+ exchanger, inhibiting Na+ absorption.
  • Cytokine LIGHT increased permeability but not Na+ absorption inhibition.
  • Phenotypic changes alone did not explain fluid secretion; increased interstitial pressure due to TNF effects on capillary permeability or smooth muscle contractility was proposed as the driving force.

Conclusions:

  • Anti-CD3 antibody and TNF induce jejunal fluid accumulation through complex mechanisms involving epithelial barrier dysfunction and altered transport.
  • While epithelial changes contribute, increased interstitial pressure is likely the primary driver of fluid secretion.
  • These findings provide insights into the pathophysiology of antibody-induced gastrointestinal inflammation.