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Related Experiment Video

Updated: May 12, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4⁺CD45RB^high T Cells into Immunodeficient Mice

Published on: April 21, 2015

Antisecretory factor suppresses intestinal inflammation and hypersecretion

E Johansson¹, E Jennische, S Lange

¹Department of Medical Microbiology and Immunology, University of Gothenburg, Sweden.

|January 1, 1998

Summary

This summary is machine-generated.

Antisecretory factor (AF) protects against intestinal inflammation and dehydration caused by bacterial toxins. This protein may offer a therapeutic approach for managing toxin-induced diarrhea.

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Published on: December 16, 2021

Area of Science:

Gastroenterology
Molecular Biology
Toxicology

Background:

Antisecretory factor (AF) is a newly discovered regulatory protein.
AF demonstrates inhibitory effects on cholera toxin-induced intestinal fluid secretion.

Purpose of the Study:

To evaluate the impact of AF on Clostridium difficile toxin A-induced inflammation and hypersecretion.
To investigate AF's effect on okadaic acid-induced morphological changes and hypersecretion in rat intestinal mucosa.

Main Methods:

Rat intestinal loops were challenged with toxin A or okadaic acid.
Recombinant AF (rAF) was administered intravenously or intraluminally before or after toxin exposure.
Morphological changes and fluid accumulation were assessed.

Main Results:

rAF treatment abolished toxin A-induced cytotoxicity and inflammation.
AF reduced intestinal fluid response to both toxin A and okadaic acid by 55-80%.
AF did not inhibit okadaic acid-induced goblet cell hyperplasia.

Conclusions:

AF shows potential in protecting against enterotoxin-induced inflammation and dehydration.
These protective effects are likely mediated through the enteric nervous system.