technique in COPD patients [14]. Levels of inflammatory cytokines had been previously shown to be elevated in induced sputum in COPD patients when stable [15]. In a cohort of COPD patients from the East London COPD study, the inflammatory markers in induced sputum were related to symptoms and physiological parameters both at baseline and at exacerbation [3]. There was a relation between exacerbation frequency and sputum cytokines, in that there was increased sputum interleukin-6 (IL-6) and IL-8 found in patients at baseline when stable with frequent exacerbations compared to those with infrequent exacerbations (Fig. 15.2), although there was no relation between cy-tokines and baseline lung function. As discussed below, exacerbations are triggered by viral infections, especially by rhinovirus, which is the cause of the common cold. Rhinovirus has been shown to increase cytokine production in an epithelial cell line [16] and thus repeated viral infection as occurs in patients with a history of frequent exacerbation may lead to up-regulation of cytokine airway expression.

There were increases at exacerbation in induced sputum IL-6 levels and the levels of IL-6 were higher when exacerbations were associated with symptoms of the common cold (Fig. 15.3). Studies where experimental rhinovirus infection has been induced in patients have found increases in sputum IL-6 in normal subjects and asthmatics [17-19]. However, rises in cell counts and IL-8 were more variable with exacerbation and not reaching statistical significance, suggesting marked heterogeneity in the degree of the inflammatory response at exacerbation. The exacerbation IL-8 levels were related to sputum neutrophil and total cell counts, indicating that neutrophil recruitment is

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