Lung mucosal immunity: immunoglobulin‐A revisited

Abstract

We read through the Review by Pilette et al. 1 with extreme interest and would like to add a contribution to the subject of airways immunity in chronic obstructive pulmonary disease (COPD). For a long time, we have witnessed, at least in Italy, the predominance of the notion that all COPD patients have a certain degree of immune deficiency as a basic pathogenetic mechanism, since they experience recurrent bronchitis exacerbations. Scientific evidence of true general or local immune defects in COPD is, in our opinion, inconclusive, although we fully agree on the point made by the authors that all the studies in the literature share methodological limitations, both in sampling and analysis techniques and in selection of patients. In our experience, different immune components can appear either similar to controls or increased (as a likely consequence of repeated stimulation by exacerbations or chronic bacterial colonization of the airways), or decreased in a specific group of COPD patients. Indeed, we recently reported decreased numbers of CD3 and CD8 lymphocytes in the bronchial biopsies of severe COPD patients, associated with an increase of neutrophils and macrophages 2. With particular regard to immunoglobulin (Ig)‐A, we found only an insignificant increase in patients with mild COPD who had never smoked 3, and a high increase in severe but clinically stable COPD patients with chronic tracheostomy and a high level of bacterial colonization 4. The experience with tracheostomized COPD patients is very interesting because they provide a model of bacteria/host interaction in which the role of immunity can be evaluated prospectively. The presence of high levels of IgA in bronchial aspirates could, in part, justify the relatively low rate of lower respiratory tract infections in these patients after discharge from hospital 5.