title: Effects of BCG infection on Schultz-Dale reaction, allergen-specific IgE levels, and Th2 immune response in sensitized rats.
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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Allergy, Department of Internal Medicine, Chonnam National University Medical School, Research Institute of Medical Science, Kwangju, Korea.
authors.forename: Y I
authors.initials: YI
authors.lastname: Koh
authors.forename: I S
authors.initials: IS
authors.lastname: Choi
authors.forename: W Y
authors.initials: WY
authors.lastname: Kim
authors.forename: H C
authors.initials: HC
authors.lastname: Lee
authors.forename: J
authors.initials: J
authors.lastname: Lee
mesh_terms: D000818:Animals; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry*; D016207:Cytokines / Q000032:analysis; D004195:Disease Models, Animal; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007114:Immunization; D007073:Immunoglobulin E / Q000032:analysis*; D008297:Male; D009163:Mycobacterium bovis / Q000276:immunology*; D011336:Probability; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D012680:Sensitivity and Specificity; D013601:T-Lymphocytes / Q000276:immunology*; D014376:Tuberculosis / Q000276:immunology* / Q000662:veterinary
chemical_list: D016207:Cytokines; D007073:Immunoglobulin E