title: Asthma, inflammation, eosinophils and bronchial hyperresponsiveness.
abstract: Asthmatics can have a blood eosinophilia which in some studies correlates with the severity of the disease. However, an increased number and percentage of activated eosinophils can be present in the blood without asthma. The eosinophils that contribute to asthma will be those in the lung. In the BAL fluids collected from asthmatics there is usually no change in total cell number, but there are changes in the differential cell count. A consistent finding is an increase in percentage of mast cells and eosinophils with a tendency for an increase in lymphocytes and epithelial cells and a decrease in percentage of macrophages. As with the blood eosinophilia, an increase in number of eosinophils can be present in BAL fluids without asthma. The site of localization and activation of the eosinophils in the lung may be critical. In bronchial biopsies, taken from asthmatics, increased number of mast cells, eosinophils and lymphocytes have been demonstrated in the bronchial mucosa together with shedding of columnar epithelial cells. However these changes have not been found, or have not reached significance, in all studies. An increase in number of activated eosinophils and T-lymphocytes has been demonstrated but an increase in number of degranulating mast cells has been disputed. A consistent finding has been thickening below the basement membrane. Attempts to correlate the changes in the BAL or lung biopsies with the severity of asthma, lung airways function or bronchial responsiveness have given inconsistent results. Treatment of asthmatics with inhaled steroids can reduce the cellular infiltration in the bronchial biopsies to normal levels but this produces a trivial reduction in bronchial responsiveness. It is possible that infiltration of inflammatory cells into the bronchial mucosa is intermittent, at least in mild asthma, but this produces changes leading to a long lasting bronchial hyperresponsiveness.
authors.affiliation: SmithKline Beecham Pharmaceuticals, Epsom, Surrey, U.K.
authors.forename: H
authors.initials: H
authors.lastname: Smith
mesh_terms: D000402:Airway Obstruction / Q000503:physiopathology; D000818:Animals; D001249:Asthma / Q000097:blood / Q000473:pathology; D001706:Biopsy; D001980:Bronchi / Q000473:pathology; D001982:Bronchial Diseases / Q000473:pathology; D001991:Bronchitis / Q000150:complications; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D004802:Eosinophilia / Q000150:complications; D004804:Eosinophils / Q000473:pathology / Q000502:physiology*; D006801:Humans; D008168:Lung / Q000473:pathology; D012130:Respiratory Hypersensitivity / Q000209:etiology / Q000473:pathology / Q000503:physiopathology