The objective of this study is to investigate whether BCG infection before, during or after sensitization
suppresses allergen-induced airway hyperresponsiveness and eosinophilic inflammation in allergic asthma
rats, and to determine the required dose of BCG to induce such an inhibition. Eighty-seven Sprague-Dawley
(SD) rats were sensitized and provoked with ovalbumin (OA). A pretreatment of 6 x 10(4) or 6 x 10(5) colony
forming units (CFUs) of BCG or saline was done at four different times: 3 days before sensitization, at
sensitization, 3 days before provocation, or at provocation. The assessment of tracheal smooth muscle
(TSM) responsiveness to electrical field stimulation or acetylcholine (ACh) and bronchoalveolar lavage
(BAL) were performed 1 day after OA provocation. Doses of 6 x 10(4) CFUs inhibited TSM sensitivity of
rats infected 3 days before sensitization or at sensitization, but not 3 days before provocation or at
provocation. However, doses of 6 x 10(5) CFUs significantly inhibited not only the airway eosinophilia
of rats infected 3 days before sensitization or at sensitization, but also the TSM sensitivity of rats
infected 3 days before provocation or at provocation. In conclusion, BCG infection suppresses the development
of sensitivity of airway smooth muscle and airway eosinophilic inflammation in allergic asthma rats.
Furthermore, a relatively high dose of BCG infection inhibits airway sensitivity, even after allergen
sensitization.
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