Lower airways inflammation is a central feature of many lung diseases, including asthma, chronic obstructive pulmonary disease (COPD) and pneumonia. Although the specific characteristics of the inflammatory responses and the site of inflammation differ between one disease to another, they always involve recruitment and activation of inflammatory cells and changes in structural cells of the lung. Inflammatory responses are associated with an increased expression of a cascade of proteins including cytokines, chemokines, growth factors, enzymes, adhesion molecules and receptors. In most cases the increased expression of these proteins is the result of enhanced gene transcription: many of these genes are not expressed in normal cells under resting conditions but they are induced in the inflammatory process in a cell-specific manner. Transcription factors regulate the expression of many pro-inflammatory genes and play a key role in the pathogenesis of airway inflammation. Many studies have suggested a role for viral infections not only as a causative agent of pneumonia but also of asthma and COPD exacerbations. In this review we will provide an overview of the relationship between common respiratory viral infections and the molecular mechanisms involved in the activation of airway inflammation and on the regulation of transcription factors in these inflammatory respiratory diseases. The relative importance of each transcription factor will be certainly greatly clarified in the next few years with the growing availability of specific inhibitors capable of blocking activation of a specific transcription factor. Clearly this is an exciting new area of ongoing research with promising therapeutic potential.

Molecular mechanisms of respiratory virus-induced asthma and COPD exacerbations and pneumonia / Caramori, Gaetano; Ito, K; Contoli, M; DI STEFANO, A; Johnston, Sl; Adcock, Im; A., Papi. - In: CURRENT MEDICINAL CHEMISTRY. - ISSN 0929-8673. - 13:19(2006), pp. 2267-2290.

Molecular mechanisms of respiratory virus-induced asthma and COPD exacerbations and pneumonia

CARAMORI, Gaetano;
2006-01-01

Abstract

Lower airways inflammation is a central feature of many lung diseases, including asthma, chronic obstructive pulmonary disease (COPD) and pneumonia. Although the specific characteristics of the inflammatory responses and the site of inflammation differ between one disease to another, they always involve recruitment and activation of inflammatory cells and changes in structural cells of the lung. Inflammatory responses are associated with an increased expression of a cascade of proteins including cytokines, chemokines, growth factors, enzymes, adhesion molecules and receptors. In most cases the increased expression of these proteins is the result of enhanced gene transcription: many of these genes are not expressed in normal cells under resting conditions but they are induced in the inflammatory process in a cell-specific manner. Transcription factors regulate the expression of many pro-inflammatory genes and play a key role in the pathogenesis of airway inflammation. Many studies have suggested a role for viral infections not only as a causative agent of pneumonia but also of asthma and COPD exacerbations. In this review we will provide an overview of the relationship between common respiratory viral infections and the molecular mechanisms involved in the activation of airway inflammation and on the regulation of transcription factors in these inflammatory respiratory diseases. The relative importance of each transcription factor will be certainly greatly clarified in the next few years with the growing availability of specific inhibitors capable of blocking activation of a specific transcription factor. Clearly this is an exciting new area of ongoing research with promising therapeutic potential.
2006
Molecular mechanisms of respiratory virus-induced asthma and COPD exacerbations and pneumonia / Caramori, Gaetano; Ito, K; Contoli, M; DI STEFANO, A; Johnston, Sl; Adcock, Im; A., Papi. - In: CURRENT MEDICINAL CHEMISTRY. - ISSN 0929-8673. - 13:19(2006), pp. 2267-2290.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/2964062
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