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Part of the book series: Respiratory Pharmacology and Pharmacotherapy ((RPP))

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Abstract

The exact cellular and molecular events leading to airways obstruction and physiological dysregulation in asthma have not been fully defined through human experimentation in vivo. Significant genetic, pathophysiological and clinical variation in the presentation and natural history of asthma complicates this experimentation. Obvious economic and ethical concerns also limit the investigation of asthma in human subjects. Nevertheless, direct examination of specimens from asthmatics has led to an important shift in our concept of the pathogenesis of this disorder. It is now widely held that asthma is a chronic inflammatory disorder and that the obstruction and airways hyperresponsiveness (AHR) that are characteristic of asthma are largely the result of this inflammatory response and its fibrotic and tissue-damaging sequellae. As a result, anti-inflammatory interventions are now the cornerstone of asthma therapy and the inflammatory mechanisms of asthma are now the major focus of research activities in this field. In spite of this insight, the role that individual mediators play in asthmatic inflammation, the fundamental molecular mechanisms leading to the chronicity of asthmatic inflamation, and the events linking inflammation, bronchoconstriction and bronchial reactivity remain important, inadequately addressed areas in the pathogenesis of this disorders.

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Schilz, R., Elias, J.A. (1996). Transgenic Animals and the Modelling of Asthma. In: Raeburn, D., Giembycz, M.A. (eds) Airways Smooth Muscle: Modelling the Asthmatic Response In Vivo . Respiratory Pharmacology and Pharmacotherapy. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-9000-7_11

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