Allergy, asthma & immunology research · 2012
Asthma Prevention by Lactobacillus Rhamnosus in a Mouse Model is Associated With CD4(+)CD25(+)Foxp3(+) T Cells.
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Jang Seong-Ok, Kim Ha-Jung, Kim Young-Joon, Kang Mi-Jin, Kwon Ji-Won, Seo Ju-Hee, Kim Hyung Young, Kim Byoung-Ju, Yu Jinho, Hong Soo-Jong
Аннотация
PURPOSE: Probiotic bacteria can induce immune regulation or immune tolerance in allergic diseases. The underlying mechanisms have been recently investigated, but are still unclear. The aim of this study was to evaluate the protective effects of the probiotic Lactobacillus rhamnosus (Lcr35) in a mouse model of asthma and to identify its mechanism of action.
METHODS: Lcr35 was administered daily by the oral route at a dosage of 1×10(9) CFU/mouse in BALB/c mice for 7 days before the first sensitization. Clinical parameters and regulatory T (Treg) cells were examined. The role of CD4(+)CD25(+)Foxp3(+) Treg cells was analyzed using a Treg cell-depleting anti-CD25 monoclonal antibody (mAb).
RESULTS: Airway hyperresponsiveness, total IgE production, pulmonary eosinophilic inflammation, and splenic lymphocyte proliferation were suppressed after Lcr35 treatment. Th1 (IFN-γ) and Th2 (IL-4, IL-5, and IL-13) cytokines in the serum were suppressed, and the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in the spleen was significantly increased in the Lcr35 treatment group. Anti-CD25 mAb administration abolished the protective effects of Lcr35, indicating that CD4(+) CD25(+)Foxp3(+) Treg cells are essential in mediating the activity of Lcr35.
CONCLUSIONS: Oral administration of Lcr35 attenuated the features of allergic asthma in a mouse model and induced immune regulation by a CD4(+)CD25(+)Foxp3(+) Treg cell-mediated mechanism.
METHODS: Lcr35 was administered daily by the oral route at a dosage of 1×10(9) CFU/mouse in BALB/c mice for 7 days before the first sensitization. Clinical parameters and regulatory T (Treg) cells were examined. The role of CD4(+)CD25(+)Foxp3(+) Treg cells was analyzed using a Treg cell-depleting anti-CD25 monoclonal antibody (mAb).
RESULTS: Airway hyperresponsiveness, total IgE production, pulmonary eosinophilic inflammation, and splenic lymphocyte proliferation were suppressed after Lcr35 treatment. Th1 (IFN-γ) and Th2 (IL-4, IL-5, and IL-13) cytokines in the serum were suppressed, and the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in the spleen was significantly increased in the Lcr35 treatment group. Anti-CD25 mAb administration abolished the protective effects of Lcr35, indicating that CD4(+) CD25(+)Foxp3(+) Treg cells are essential in mediating the activity of Lcr35.
CONCLUSIONS: Oral administration of Lcr35 attenuated the features of allergic asthma in a mouse model and induced immune regulation by a CD4(+)CD25(+)Foxp3(+) Treg cell-mediated mechanism.