| Asthma is a worldwide health problem and leading cause of childhood morbidity. The increasing prevalence of asthma places importance on understanding the biological mechanisms behind this complex disease. Considerable evidence suggests that asthma originates early in life. Environmental allergen exposures acting on a genetic background susceptible to asthma, may modify innate patterns of respiratory development and gene expression, facilitating the initiation of disease. The origins of asthma susceptibility and the influence of in utero allergen exposure on respiratory development were studied in rat models of atopy (Brown Norway [BN]) and airway hyperresponsiveness (Fisher). BN animals demonstrated increased epithelial proliferation, goblet cell hyperplasia, elevated eosinophils and IgE levels. Fisher rats displayed increased lung resistance and elevated neutrophils. The distinct respiratory phenotypes and gene expression patterns demonstrated were impacted by in utero allergen exposure, influencing asthma susceptibility. Studying causes of asthma susceptibility during this critical period has implications for asthma treatment and prevention. |
