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  • Title: [Inflammatory mechanisms of bronchial asthma].
    Author: Pujol JL, Godard P, Bousquet J, Michel FB.
    Journal: Rev Mal Respir; 1987; 4(3):111-20. PubMed ID: 3303200.
    Abstract:
    The definition of asthma brings with it the idea of inflammation, as bronchial obstruction, which characterises it, is associated with bronchospasm, hypersecretion and oedema. In the asthmatic, awareness of the bronchial inflammation at the time of diagnosis is essential, as it contributes to prognosis and therapeutic orientation. The diagnosis of bronchial inflammation begins with the clinical assessment, such as cough, expectoration and the worsening of symptoms in the morning alerts the clinician. In the course of certain clinical forms of asthma the absence of any relief of airflow obstruction by bronchodilators, although it is proved to be reversible after a few days of glucocorticoids, is evidence of inflammation. Fibreoptic bronchoscopy extends the clinical examination and enables a direct observation of airways inflammation. In addition it allows sampling, such as bronchial biopsy and/or broncho-alveolar lavage. The mechanism of bronchial inflammation are well understood; some mastocytes (mucous) are present in the broncho-alveolar contents and are probably the origin of inflammatory reaction, whether the stimulus be allergenic or not. The mediators liberated lead in part to the bronchial obstruction but equally to cellular recruitment and thus to an amplification of the initial reaction. Probably the eosinophils play a fundamental role ar this stage. The alveolar macrophages are equally implicated in this inflammatory reaction. Bronchial inflammation appears as a result of complex cellular reactions, regulated by chemical mediators. The most obvious consequence of bronchial inflammation is the delayed bronchial reaction. The experimental model contributes to physio-pathological understanding and a characterisation of the inflammatory components is observed principally in those patients with severe asthma. Agents capable of causing or aggravating bronchial hyper-reactivity can also induce bronchial inflammation. From this observation the idea is born of a relation between the concept of bronchial hyper-reactivity and bronchial inflammation. Acquired bronchial hyper-reactivity evolves in parallel to the symptoms and its intensity is correlated with the severity of the asthma. An understanding of the inflammatory mechanisms without doubt will bring new therapeutic perspectives.
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