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• W2093664169 abstract "Controversy still exists as to whether gastrointestinal colonisation by Candida albicans contributes to aggravation of atopic dermatitis. We hypothesised that Candida colonisation promotes food allergy, which is known to contribute to a pathogenic response in atopic dermatitis. We tested this using a recently established murine Candida colonisation model.Candida colonisation in the gastrointestinal tract was established by intragastric inoculation with C albicans in mice fed a synthetic diet. To investigate sensitisation against food antigen, mice were intragastrically administered with ovalbumin every other day for nine weeks, and antiovalbumin antibody titres were measured weekly. To examine gastrointestinal permeation of food antigen, plasma concentrations of ovalbumin were measured following intragastric administration of ovalbumin.Ovalbumin specific IgG and IgE titres were higher in BALB/c mice with Candida colonisation than in normal mice. Gastrointestinal permeation of ovalbumin was enhanced by colonisation in BALB/c mice. Histological examination showed that colonisation promoted infiltration and degranulation of mast cells. Candida colonisation did not enhance ovalbumin permeation in mast cell deficient W/Wv mice but did in congenic littermate control +/+ mice. Reconstitution of mast cells in W/Wv mice by transplantation of bone marrow derived mast cells restored the ability to increase ovalbumin permeation in response to Candida colonisation.These results suggest that gastrointestinal Candida colonisation promotes sensitisation against food antigens, at least partly due to mast cell mediated hyperpermeability in the gastrointestinal mucosa of mice." @default.
• W2093664169 created "2016-06-24" @default.
• W2093664169 creator A5061068865 @default.
• W2093664169 date "2006-02-16" @default.
• W2093664169 modified "2023-09-27" @default.
• W2093664169 title "Gastrointestinal Candida colonisation promotes sensitisation against food antigens by affecting the mucosal barrier in mice" @default.
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• W2093664169 doi "https://doi.org/10.1136/gut.2005.084954" @default.
• W2093664169 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1856330" @default.
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