American journal of respiratory and critical care medicine
-
Am. J. Respir. Crit. Care Med. · Nov 2001
Randomized Controlled Trial Clinical TrialRhinovirus-induced airway inflammation in asthma: effect of treatment with inhaled corticosteroids before and during experimental infection.
Asthma exacerbations are frequently linked to rhinovirus infections. However, the associated inflammatory pathways are poorly understood, and treatment of exacerbations is often unsatisfactory. In the present study we investigated whether antiinflammatory treatment with inhaled corticosteroids prevents any rhinovirus-induced worsening of lower airway inflammation. ⋯ Yet it did not significantly affect the RV16-associated changes in the numbers of any of the inflammatory cell types. We conclude that RV16 infection by itself induces only subtle worsening of airway inflammation in asthma, which is not improved (or worsened) by inhaled corticosteroids. The latter finding is in keeping with the limited protection of inhaled corticosteroids against acute asthma exacerbations.
-
Am. J. Respir. Crit. Care Med. · Nov 2001
Review Comparative StudyRemodeling in response to infection and injury. Airway inflammation and hypersecretion of mucus in smoking subjects with chronic obstructive pulmonary disease.
Airway epithelium represents the first line of defense against toxic inhalants. In some subjects, cigarette smoking causes airway inflammation, hypersecretion of mucus, and poorly reversible airflow limitation through mechanisms that are still largely unknown. Likewise, it is unclear why only some smokers develop chronic obstructive pulmonary disease (COPD). ⋯ Mucus is produced by bronchial glands and goblet cells lining the airway epithelium. Unlike mucous gland enlargement, greater mucosal inflammation is associated with sputum production. Whereas neutrophil infiltration of submucosal glands occurs only in smokers with COPD, goblet cell hyperplasia in peripheral airways occurs both in smokers with or without COPD, suggesting that the major determinant of goblet cell hyperplasia is cigarette smoke itself.
-
Am. J. Respir. Crit. Care Med. · Nov 2001
Review Comparative StudyRole of latent viral infections in chronic obstructive pulmonary disease and asthma.
Acute viral respiratory tract infections are well known to precipitate asthma attacks and acute exacerbations of chronic obstructive pulmonary disease, but their role in the pathogenesis of chronic disease is poorly defined. Double-stranded DNA viruses have the ability to persist in airway epithelial cells long after the acute infection has cleared. During these latent infections, viral genes are expressed at the protein level without replication of a complete virus. ⋯ Furthermore, this infection independently increased the number of CD-8 cells, whereas the cigarette smoke independently increased the number of CD-4 cells in the inflammatory infiltrate. On the other hand, allergen-induced lung inflammation was uninfluenced by latent adenoviral infection in the guinea pig, but the latent infection caused the eosinophilic component of this response to become steroid resistant. These studies suggest that latent adenoviral infections may have a role in the pathogenesis of obstructive airway disease by amplifying the response to cigarette smoke and inducing steroid resistance.