ABSTRACT
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.
Subject(s)
Male , Rats , Animals , Asthma/immunology , BCG Vaccine/immunology , Disease Models, Animal , Disease Models, Animal , Eosinophils/immunology , Leukocyte Count , Lung/immunology , Muscle, Smooth, Vascular/immunology , Rats, Sprague-Dawley , Time Factors , VaccinationABSTRACT
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.
Subject(s)
Male , Rats , Animals , Asthma/immunology , BCG Vaccine/immunology , Disease Models, Animal , Disease Models, Animal , Eosinophils/immunology , Leukocyte Count , Lung/immunology , Muscle, Smooth, Vascular/immunology , Rats, Sprague-Dawley , Time Factors , VaccinationABSTRACT
BACKGROUND: Portable devices for measuring peak expiratory flow(PEF) are now of proved value in the diagnosis and management of asthma and many lightweight PEF meters have become available. However, it is necessary to determine whether peak expiratory flow rate(PEFR) measurements measured with peak flowmeters is accurate and reproducible for clinical application. The aim of the present study is to define accuracy, agreement, and precision of mini-Wright peak flow meter(MPFM) against standard pneumotachygraph. METHODS: The lung function tests by standard pneumotachygraph and PEFR measurement by MPFM were performed in a random order for 2 hours in 22 normal and 17 asthmatic subjects and also were performed for 3 successive days in 22 normals. RESULTS: The PEFR measured with MPFM was significantly related to the PEFR and FEV1 measured with standard pneumotachygraph in normal and asthmatics(for PEFR, r=0.92 p0.05) and the coefficient of variation(2.4 1.2%) of PEFR measured with MPFM was significantly lower than that( 5.2 3.5%) with standard pneurnotachygraph in normal (p<0.05). CONCLUSION: This results suggest that the MPFM was as accurate and reproducible as standard pneumotachygraph for monitoring of PEFR in the asthmatic subjects.