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Pacific oyster-derived polysaccharides attenuate allergen-induced intestinal inflammation in a murine model of food allergy

Oyster-derived polysaccharides (OPS) have been shown to modulate the T helper (Th)1/Th2 immunobalance toward the Th1-dominant direction in antigen-primed splenocytes. In the present study, we hypothesized that OPS might attenuate intestinal inflammation associated with food allergy, a Th2-dominant i...

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Detalles Bibliográficos
Autores principales: Cheng, Chiung-Hsiang, Wu, Hsin-Ying, Wu, Chi-Fang, Jan, Tong-Rong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taiwan Food and Drug Administration 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9345417/
https://www.ncbi.nlm.nih.gov/pubmed/28911394
http://dx.doi.org/10.1016/j.jfda.2015.08.006
Descripción
Sumario:Oyster-derived polysaccharides (OPS) have been shown to modulate the T helper (Th)1/Th2 immunobalance toward the Th1-dominant direction in antigen-primed splenocytes. In the present study, we hypothesized that OPS might attenuate intestinal inflammation associated with food allergy, a Th2-dominant immune disorder. BALB/c mice were sensitized twice with ovalbumin (OVA) absorbed to alum and then repeatedly challenged with intragastric OVA to induce intestinal allergic responses. The mice were administered by gavage with OPS and/or vehicle (distilled water) once/d during the two sensitization phases, and once every other day during the challenge phase. Administration with OPS attenuated OVA challenge-elicited diarrhea, and the infiltration of mast cells in the intestine. OPS demonstrated a protective effect on the reduced ratio of villus length over crypt depth of the intestine in allergic mice. Furthermore, OPS administration markedly attenuated the intestinal expression of the Th2 signature cytokine interleukin-4 (IL-4). Collectively, these results demonstrated the in vivo antiallergic activity of OPS, which is associated with the suppression of allergen-induced intestinal Th2 responses and mast cell activation.