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Updated: Jul 5, 2026

Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach
Published on: May 2, 2018
Bacterial lipopolysaccharide-induced intestinal microvascular lesions leading to acute diarrhea
V I Mathan1, G R Penny, M M Mathan
1Wellcome Research Unit, Christian Medical College Hospital, Vellore, India.
Abstract:
Subcutaneous challenge of mice with lipopolysaccharide (LPS) from gram negative bacteria, produced an intestinal microvascular lesion causing fluid exudation into the lumen of the intestine and diarrhea. The microvascular lesion was characterized by endothelial cell damage and microthrombi in the venules and capillaries of the intestinal lamina propria. Marker organisms, given orally to challenged mice, grew in the exuded fluid and could invade the mucosa. Intravenous transfer of postchallenge plasma produced the lesion in normal mice and absorption of such plasma by Sepharose coupled to LPS-antibody abolished this effect. Instillation of large quantities of LPS into the lumen of the intestine produced scattered microvascular lesions, although none of these animals developed diarrhea. Since a similar microvascular lesion has been described in the rectal mucosal lamina propria of adults with acute diarrhea, it is suggested that LPS-induced vascular damage may be a novel mechanism in the pathogenesis of acute diarrhea.
Insights
Lipopolysaccharide (LPS) from gram-negative bacteria causes intestinal damage and diarrhea in mice. This vascular damage mechanism may be a novel pathway in acute diarrhea.
Area of Science:
- Microbiology
- Immunology
- Pathology
Background:
- Gram-negative bacteria possess lipopolysaccharide (LPS), a potent endotoxin.
- Intestinal microvascular lesions are implicated in acute diarrhea pathogenesis.
Purpose of the Study:
- To investigate the role of LPS in inducing intestinal microvascular lesions and diarrhea.
- To elucidate the mechanism of LPS-induced intestinal damage.
Main Methods:
- Subcutaneous LPS challenge in mice.
- Oral administration of marker organisms.
- Intravenous plasma transfer experiments.
- Sepharose-LPS-antibody absorption assays.
Main Results:
- Subcutaneous LPS challenge induced intestinal microvascular lesions, characterized by endothelial cell damage and microthrombi, leading to fluid exudation and diarrhea.
- Marker organisms invaded the mucosa in challenged mice.
- Plasma from challenged mice transferred the lesion to normal mice, an effect abolished by LPS-antibody absorption.
- Intraluminal LPS induced scattered lesions but not diarrhea.
Conclusions:
- LPS-induced microvascular damage is a potential mechanism in acute diarrhea pathogenesis.
- The findings suggest a novel pathway for LPS-mediated intestinal injury.
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