Germ-free status and altered caecal subdominant microbiota are associated with a high susceptibility to cow's milk allergy in mice.
FEMS Microbiol Ecol
; 76(1): 133-44, 2011 Apr.
Article
en En
| MEDLINE
| ID: mdl-21223329
Studies suggesting that the development of atopy is linked to gut microbiota composition are inconclusive on whether dysbiosis precedes or arises from allergic symptoms. Using a mouse model of cow's milk allergy, we aimed at investigating the link between the intestinal microbiota, allergic sensitization, and the severity of symptoms. Germ-free and conventional mice were orally sensitized with whey proteins and cholera toxin, and then orally challenged with ß-lactoglobulin (BLG). Allergic responses were monitored with clinical symptoms, plasma markers of sensitization, and the T-helper Th1/Th2/regulatory-T-cell balance. Microbiota compositions were analysed using denaturing gradient gel electrophoresis and culture methods. Germ-free mice were found to be more responsive than conventional mice to sensitization, displaying a greater reduction of rectal temperature upon challenge, higher levels of blood mouse mast cell protease-1 (mMCP-1) and BLG-specific immunoglobulin G1 (IgG1), and a systemic Th2-skewed response. This may be explained by a high susceptibility to release mMCP-1 even in the presence of low levels of IgE. Sensitization did not alter the microbiota composition. However, the absence of or low Staphylococcus colonization in the caecum was associated with high allergic manifestations. This work demonstrates that intestinal colonization protects against oral sensitization and allergic response. This is the first study to show a relationship between alterations within the subdominant microbiota and severity of food allergy.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Ciego
/
Hipersensibilidad a la Leche
/
Metagenoma
/
Proteínas de la Leche
Tipo de estudio:
Risk_factors_studies
Límite:
Animals
Idioma:
En
Revista:
FEMS Microbiol Ecol
Año:
2011
Tipo del documento:
Article
País de afiliación:
Francia
Pais de publicación:
Reino Unido