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Lung mucosal immunity: immunoglobulin-A revisited

Salvatore Maugeri Foundation, IRCCS, Scientific Institute of Rehabilitation, Division of Pulmonary Disease, Veruno, NO, Italy

To the Editor:

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.

We appreciated the long and accurate list of defence mechanisms in the respiratory tract reported by the authors, which clearly shows that specific immune functions are only a part of the airways protection system. Indirect proof that immunoglobulins are only a part, albeit an important part, of mucosal immunity, comes from studies on the stimulation of mucosa-associated lymphoid tissues with oral vaccines or bacterial extracts, which have been demonstrated to reduce the impact of bronchitis exacerbations, at least in mild-to-moderate chronic obstructive pulmonary disease 6. The mechanisms of action were reflected in an increase of immunoglobulin-A in the airways' fluids, but more solid evidence, from a biological point of view, was the activation of alveolar macrophages 7. In our opinion, the potential of oral bacterial extracts to stimulate immunoglobulin-A production in the airways should be further investigated. In conclusion, we would once again like to stress that the impairment of defence systems in the airways is not simply a question of specific immunity, and that a clinically relevant imbalance in chronic obstructive pulmonary disease must be evaluated within a complex defence network concept, rather than in a simple cause/effect perspective.

References

1. Pilette C, Ouadrhiri Y, Godding V, Vaerman J-P, Sibille Y. Lung mucosal immunity: immunoglobulin-A revisited. Eur Respir J 2001;18:571–588.[Abstract/Free Full Text]
2. Di Stefano A, Capelli A, Lusuardi M, et al. Decreased T lymphocyte infiltration in bronchial biopsies of subjects with severe chronic obstructive pulmonary disease. Clin Exp Allergy 2001;31:893–902.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
3. Lusuardi M, Capelli A, Cerutti CG, Spada EL, Donner CF. Airways inflammation in subjects with chronic bronchitis who have never smoked. Thorax 1994;49:1211–1216.[Abstract/Free Full Text]
4. Lusuardi M, Capelli A, Cerutti CG, Gnemmi I, Zaccaria S, Donner CF. Influence of clinical history on airways bacterial colonization in subjects with chronic tracheostomy. Respir Med 2000;94:436–440.[CrossRef][Web of Science][Medline] [Order article via Infotrieve]
5. Harlid R, Andersson G, Frostell CG, Jorbeck HJA, Ortqvist AB. Respiratory tract colonization and infection in patients with chronic tracheostomy. A one-year study in patients living at home. Am J Respir Crit Care Med 1996;154:124–129.[Abstract]
6. Bergemann R, Brandt A, Zoellner U, Donner CF. Preventive treatment of chronic bronchitis: a meta-analysis of clinical trials with a bacterial extract (OM-85 BV) and a cost-effectiveness analysis. Monaldi Arch Chest Dis 1994;49:302–307.[Medline] [Order article via Infotrieve]
7. Lusuardi M, Capelli A, Carli S, Spada EL, Spinazzi A, Donner CF. Local airways immune modifications induced by oral bacterial extracts in chronic bronchitis. Chest 1993;103:1783–1791.[Abstract/Free Full Text]

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