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Induction of colitis in mice with food allergen-specific immune response

View Article: PubMed Central - PubMed

ABSTRACT

The pathogenesis of intestinal chronic inflammation is unclear. Food allergy plays an important role in the induction of intestinal inflammation. This study aims to test a hypothesis that food allergy initiates colitis. In this study, BALB/c mice were sensitized to a common food allergen, ovalbumin (OVA) with cholera toxin (CT) as an adjuvant. The colon epithelial barrier function was assessed with Ussing chamber technique. Expression of T cell immunoglobulin mucin domain molecule-4 (TIM4) in dendritic cells was evaluated by flow cytometry, RT-PCR and Western blotting. The results showed that allergen-related colitis was induced in mice as shown by heavy infiltration of inflammatory cells in the colon mucosa, loss of body weight of mice, increases in myeloperoxidase, tumor necrosis factor-α, interleukin-4, OVA-specific IgE in the colon tissue. The colon epithelial barrier function was markedly compromised in colitis group mice, which was mimicked by exposure the colon mucosa to CT in Ussing chamber. High frequency of TIM4+ dendritic cells was detected in the colon mucosa of colitis mice. Exposure of dendritic cells to CT markedly increased the expression of TIM4. We conclude that IBD-like inflammation can be induced in the mouse colon by the food allergen-related immune response.

No MeSH data available.


Related in: MedlinePlus

Exposure to CT compromises colon epithelial barrier function.The bars indicate the Isc (A) conductance (B) and colon epithelial layer permeability to OVA (C) Colitis: Samples were from colitis group. CT: Cholera toxin concentrations in the epithelial side of Ussing chambers, at where the samples were from control group. *p < 0.01, compared with the colitis group. Each group consists of 6 mice.
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f4: Exposure to CT compromises colon epithelial barrier function.The bars indicate the Isc (A) conductance (B) and colon epithelial layer permeability to OVA (C) Colitis: Samples were from colitis group. CT: Cholera toxin concentrations in the epithelial side of Ussing chambers, at where the samples were from control group. *p < 0.01, compared with the colitis group. Each group consists of 6 mice.

Mentions: We next observed the effect of CT on facilitating OVA to be transported across colon epithelial barrier. Colon segments were collected from colitis mice and control mice and mounted on Ussing chambers. Isc, conductance and permeability to OVA (labeled with FITC) were recorded following our established procedures10. As shown by Fig. 4, the levels of Isc, conductance and permeability to OVA were significantly higher in the colitis group than in the control group (the “0” group). Exposure of colon tissue from control mice to CT in Ussing chambers markedly increased the levels of Isc, conductance and permeability to OVA in a CT dose-dependent manner. The results demonstrate that exposure to CT compromises the colon epithelial barrier function and facilitates the absorption of allergen.


Induction of colitis in mice with food allergen-specific immune response
Exposure to CT compromises colon epithelial barrier function.The bars indicate the Isc (A) conductance (B) and colon epithelial layer permeability to OVA (C) Colitis: Samples were from colitis group. CT: Cholera toxin concentrations in the epithelial side of Ussing chambers, at where the samples were from control group. *p < 0.01, compared with the colitis group. Each group consists of 6 mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5015191&req=5

f4: Exposure to CT compromises colon epithelial barrier function.The bars indicate the Isc (A) conductance (B) and colon epithelial layer permeability to OVA (C) Colitis: Samples were from colitis group. CT: Cholera toxin concentrations in the epithelial side of Ussing chambers, at where the samples were from control group. *p < 0.01, compared with the colitis group. Each group consists of 6 mice.
Mentions: We next observed the effect of CT on facilitating OVA to be transported across colon epithelial barrier. Colon segments were collected from colitis mice and control mice and mounted on Ussing chambers. Isc, conductance and permeability to OVA (labeled with FITC) were recorded following our established procedures10. As shown by Fig. 4, the levels of Isc, conductance and permeability to OVA were significantly higher in the colitis group than in the control group (the “0” group). Exposure of colon tissue from control mice to CT in Ussing chambers markedly increased the levels of Isc, conductance and permeability to OVA in a CT dose-dependent manner. The results demonstrate that exposure to CT compromises the colon epithelial barrier function and facilitates the absorption of allergen.

View Article: PubMed Central - PubMed

ABSTRACT

The pathogenesis of intestinal chronic inflammation is unclear. Food allergy plays an important role in the induction of intestinal inflammation. This study aims to test a hypothesis that food allergy initiates colitis. In this study, BALB/c mice were sensitized to a common food allergen, ovalbumin (OVA) with cholera toxin (CT) as an adjuvant. The colon epithelial barrier function was assessed with Ussing chamber technique. Expression of T cell immunoglobulin mucin domain molecule-4 (TIM4) in dendritic cells was evaluated by flow cytometry, RT-PCR and Western blotting. The results showed that allergen-related colitis was induced in mice as shown by heavy infiltration of inflammatory cells in the colon mucosa, loss of body weight of mice, increases in myeloperoxidase, tumor necrosis factor-&alpha;, interleukin-4, OVA-specific IgE in the colon tissue. The colon epithelial barrier function was markedly compromised in colitis group mice, which was mimicked by exposure the colon mucosa to CT in Ussing chamber. High frequency of TIM4+ dendritic cells was detected in the colon mucosa of colitis mice. Exposure of dendritic cells to CT markedly increased the expression of TIM4. We conclude that IBD-like inflammation can be induced in the mouse colon by the food allergen-related immune response.

No MeSH data available.


Related in: MedlinePlus