Taurine administration prevents the intestine from the damage induced by beta-lactoglobulin sensitization in a murine model of food allergy

Publication date: Available online 27 September 2018

Source: Allergologia et Immunopathologia

Author(s): S. Aïnad-Tabet, H. Grar, A. Haddi, H. Negaoui, A. Guermat, O. Kheroua, D. Saïdi

Abstract

Background

Allergy to cow's milk proteins has often been associated with dysfunction of the intestinal mucosa caused by chronic inflammation in infants. This study evaluated the protective effect of taurine on intestinal damage induced by beta-lactoglobulin (β-Lg) in Balb/c mice used as an animal model of allergy to cow's milk proteins.

Methods

Balb/c mice were treated with taurine administered orally by gavage (3 mmol/kg/day) or intraperitoneally (100 mg/kg/day) for two weeks, then sensitized intraperitoneally with β-Lg. The electrophysiological parameters: active ion transport of chloride (Short-circuit current: Isc) and the passive ion permeability (Conductance: G) were measured ex vivo in Ussing chamber by intestine challenge with β-Lg. Histological study was used to assess gut inflammation. Serum levels of TNF-α and IL-6 were measured. Serum IgG and IgE anti-β-Lg were determined by ELISA.

Results

Compared with sensitized mice, β-Lg challenge of intestinal epithelium of taurine-pre-treated mice in Ussing chamber did not influence the intensity of Isc, nor produce any changes in the G, reflecting a reduction in the secretory response and epithelial permeability. Histological and morphometric analysis showed that taurine reduced the intestinal damage and limited intestine retraction caused by β-Lg sensitization. No statistically significant difference in the serum levels of TNF-α or IL-6 was found after oral or intraperitoneal administration of taurine. Treatment with taurine significantly decreased the IgG (p < 0.001) and IgE anti β-Lg levels (p < 0.05).

Conclusions

These results have for the first time provided evidence that pre-treatment with taurine appears to prevent intestinal damage induced by β-Lg.

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