Although eosinophilic airway inflammation is recognized as an important feature of some patients with chronic, stable asthma, evidence supports an important role of neutrophils in acute exacerbations. In stable asthma, there is typically an infiltrate of eosinophils, which occurs in response to cytokines such as interleukin (IL)-5, secreted by
T-helper type 2 lymphocytes. In contrast, during acute exacerbations of asthma, the airway inflammatory response is both more intense and heterogeneous. The increased intensity of airway inflammation is reflected by an elevated total cell count in sputum. The heterogeneity of the inflammatory response is reflected by an increase in neutrophils as well as eosinophils, and there are reports of exacerbations without sputum eosinophilia. There is also evidence for increased expression of the potent neutrophil chemoattractant IL-8, in addition to the presence of IL-5. There is heterogeneity in the concentrations of IL-8 in patients with moderate asthma and the strong correlation between the concentration of IL-8 release by peripheral blood mononuclear cells and the frequency of asthma exacerbations. Buy asthma inhalers online to arrest asthma attacks (read about Ventolin and Flovent) .
Leukocytes, particularly neutrophils and eosinophils, are the first cells recruited to the site of tissue damage after an inflammatory insult. These cells are then removed by apoptosis during the resolution of the inflammatory response. Neutrophils are the predominant inflammatory leukocyte characterizing airway inflammation in acute severe asthma, and this may influence the clinical presentation, predisposing to a sudden severe attack. IL-8 is a key chemokine involved in the recruitment of neutrophils to the area of inflammation, but few studies have characterized the kinetics of IL-8 production in sputum over a period of time prior to the onset of a clinical asthma exacerbation. Because it is not possible to obtain this information prospectively with a naturally occurring exacerbation, we induced loss of control of asthma by withdrawing inhaled corticosteroids so that we were able to make prospective measurements of inflammatory indexes in induced sputum. This was done in a double-blind controlled manner so that steroid withdrawal could be compared with continued therapy with inhaled corticosteroids.