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  • Title: Effects of BCG infection on Schultz-Dale reaction, allergen-specific IgE levels, and Th2 immune response in sensitized rats.
    Author: Koh YI, Choi IS, Kim WY, Lee HC, Lee J.
    Journal: Korean J Intern Med; 2001 Sep; 16(3):180-6. PubMed ID: 11769577.
    Abstract:
    BACKGROUND: BCG, a potent inducer of Th1 immune response, has been suggested to suppress Th2 response which is known to mediate IgE-mediated allergic disorders, in particular allergic asthma. Schultz-Dale reaction is known to be a model of IgE-mediated hypersensitivity. This study was done to investigate whether BCG infection suppresses the Schultz-Dale reaction by inhibiting Th2 response and allergen-specific IgE production. METHODS: Twenty-four Sprague-Dawley rats were sensitized and provoked with ovalbumin (OVA). A pretreatment of 6 x 10(4) colony forming units of BCG or saline was done 7 days before sensitization. The Schultz-Dale reaction was represented as tracheal smooth muscle contractions to 50 micrograms/mL OVA challenge in vitro. Serum OVA-specific IgE levels and IFN-gamma and IL-4 concentrations in bronchoalveolar lavage fluid (BALF) were measured. RESULTS: The Schultz-Dale reaction and serum OVA-specific IgE levels were significantly decreased in BCG infected and OVA sensitized rats compared with only sensitized rats (p < 0.01 and p < 0.05, respectively). As compared with only sensitized rats, IL-4 concentration and a ratio of IFN-gamma:IL-4 in BCG infected and OVA sensitized rats were significantly decreased (p < 0.001) and increased (p < 0.05), respectively. The Schultz-Dale reaction was correlated with OVA-specific IgE levels (r = 0.50, p < 0.05), IL-4 concentration (r = 0.69, p < 0.001), and ratio of IFN-:IL-4 (r = -0.44, p < 0.05). OVA-specific IgE levels were correlated with IL-4 concentration (r = 0.61, p < 0.01) and ratio of IFN-gamma:IL-4 (r = -0.48, p < 0.05). CONCLUSION: These findings suggest that BCG infection prior to allergen sensitization may inhibit Schultz-Dale reaction developed in the sensitized rat tracheal smooth muscle via the suppressive effects of Th2 immune response and allergen-specific IgE production.
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