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Updated: May 29, 2026
An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
Published on: December 3, 2020
Persistent epithelial barrier alterations in a rat model of postinfectious gut dysfunction
J A Fernández-Blanco1, S Barbosa, F Sánchez de Medina
1Department of Cell Biology, Physiology and Immunology, Veterinary School, Universidad Autónoma de Barcelona, Barcelona, Spain.
Background:
Mucosal mast cells (MMCs), epithelial barrier function (EBF) and the enteric nervous system (ENS) are interactive factors in the pathophysiology of functional gastrointestinal disorders. We characterized postinfectious EBF alterations in the Trichinella spiralis infection model of MMC-dependent intestinal dysfunction in rats.
Methods:
Sprague-Dawley rats were infected with T. spiralis. 30 ± 2 days postinfection, jejunal EBF (electrophysiological parameters, fluorescein isothiocyanate-dextran fluxes and responses to secretagogues and MMC degranulators) was evaluated (Ussing chamber). In some experiments, participation of secretomotor neurons was examined by tetrodotoxin (TTX) pretreatment. Jejunal histology and MMC count and activity were also assessed.
Key Results:
30 ± 2 days postinfection, when only a low grade inflammation was observed, increased MMC number and activity were associated with altered EBF. EBF alterations were characterized by increased mucosal permeability and ion secretion. In T. spiralis-infected animals, secretory responses to serotonin (5-HT) and immunoglobulin E (IgE)-dependent activation of MMCs were reduced. In contrast, responses to substance P (SP) and capsaicin were similar in infected and noninfected animals. Neuronal blockade with TTX altered secretory responses to SP and capsaicin only in infected rats.
Conclusions & Inferences:
Trichinella spiralis infection in rats, at late stages, results in persistent postinfectious intestinal barrier dysfunctions and mucosal mastocytosis, with other signs suggestive of a low grade inflammation. The altered permeability and the TTX-independent hyporesponsiveness to 5-HT and IgE indicate epithelial alterations. Changes in responses to SP and capsaicin after neuronal blockade suggest an ENS remodeling during this phase. Similar long-lasting neuro-epithelial alterations might contribute to the pathophysiology of functional and postinfectious gastrointestinal disorders.
Insights
Trichinella spiralis infection causes lasting intestinal barrier dysfunction and mucosal mastocytosis in rats. These changes, including altered epithelial and enteric nervous system function, may contribute to functional gastrointestinal disorders.
Area of Science:
- Gastroenterology
- Immunology
- Neuroscience
Background:
- Functional gastrointestinal disorders involve interactions between mucosal mast cells (MMCs), epithelial barrier function (EBF), and the enteric nervous system (ENS).
- Investigating postinfectious EBF alterations in a rat model of MMC-dependent intestinal dysfunction caused by Trichinella spiralis infection.
Purpose of the Study:
- To characterize long-term changes in intestinal barrier function and associated cellular responses following Trichinella spiralis infection.
- To elucidate the roles of MMCs, EBF, and ENS in the pathophysiology of post-infectious gastrointestinal dysfunction.
Main Methods:
- Rats were infected with T. spiralis, and jejunal EBF was assessed 30 days postinfection using Ussing chamber techniques.
- Electrophysiological parameters, fluorescein isothiocyanate-dextran fluxes, and responses to secretagogues and MMC degranulators were measured.
- Histology, MMC counts, and neuronal involvement (using tetrodotoxin) were also evaluated.
Main Results:
- Late-stage T. spiralis infection (30 days postinfection) showed increased MMC number and activity, correlating with altered EBF, including increased permeability and ion secretion.
- Secretory responses to serotonin (5-HT) and immunoglobulin E (IgE) were reduced, indicating epithelial alterations.
- Responses to substance P (SP) and capsaicin were altered after neuronal blockade (tetrodotoxin), suggesting enteric nervous system remodeling.
Conclusions:
- Persistent postinfectious intestinal barrier dysfunctions and mucosal mastocytosis occur late after T. spiralis infection in rats.
- Altered permeability and hyporesponsiveness to 5-HT and IgE point to epithelial changes, while altered responses to SP and capsaicin suggest ENS remodeling.
- These long-lasting neuro-epithelial alterations may contribute to the pathophysiology of functional and postinfectious gastrointestinal disorders.
