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Dendritic Cell Maturity and Obstructive Airway Disease

We read with great interest the letter by Tsoumakidou and Jeffery regarding our article on the accumulation of dendritic cells (DCs) in the small airways of patients with chronic obstructive pulmonary disease (COPD) (1). They suggest that DC maturation is attenuated in healthy smokers and in smokers with obstructive airway disease. This hypothesis surely deserves further attention, but our data do not allow confirmation of this statement.

When comparing data from different studies, several methodological issues need to be kept in mind. First, the site of sampling might differ. Findings in large airways are not necessarily the same as in small airways. Second, the study population might be quite different in one study compared with another. The effects of cigarette smoke on DC maturation might be different in asthmatics when compared with patients with COPD or healthy controls. Third, differences in the use of markers to study DCs are of great importance. Both CD1a and Langerin are markers for immature DCs. In the study by Tsoumakidou and colleagues, there was no effect of cigarette smoking on the number of CD1a⁺ DCs in bronchial epithelium (2), findings that are consistent with our data obtained in patients with COPD. CD83 is often used as a marker for mature DCs, but several groups reported the expression of CD83 on B lymphocytes and Langerhans' cells (3). Immunohistochemical studies using CD83 as a single marker to identify mature DCs should be interpreted with caution. CD208 may be a better marker to study mature DCs by immunohistochemistry (4).

There are currently no data that allow a conclusion on the effect of cigarette smoke on DC maturation in small airways of patients with COPD. Future cross-sectional studies should be undertaken to investigate the effect of cigarette smoking on both immature and mature DC numbers in healthy controls, patients with COPD, and asthmatics. The subjects in these studies should be carefully matched regarding age, severity of disease, site of sampling, and treatment. Finally, it would be especially useful to start longitudinal studies in which the number of DCs could be evaluated before and after quitting smoking. While this is not possible on tissue sections from surgical specimens, it should be possible to perform these studies using serial bronchial biopsies.

Ingel K. Demedts, Guy F. Joos and Guy G. Brusselle

Ghent University Hospital, Ghent, Belgium

FOOTNOTES

Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

1. Demedts IK, Bracke KR, Pottelberge GV, Testelmans D, Verleden GM, Vermassen FE, Joos GF, Brusselle GG. Accumulation of dendritic cells and increased CCL20 levels in the airways of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2007;175:998–1005.[Abstract/Free Full Text]
2. Tsoumakidou M, Elston W, Zhu J, Wang Z, Gamble E, Siafakas NM, Barnes NC, Jeffery PK. Cigarette smoking alters bronchial mucosal immunity in asthma. Am J Respir Crit Care Med 2007;175:919–925.[Abstract/Free Full Text]
3. Zhou LJ, Schwarting R, Smith HM, Tedder TF. A novel cell-surface molecule expressed by human interdigitating reticulum cells, Langerhans cells, and activated lymphocytes is a new member of the Ig superfamily. J Immunol 1992;149:735–742.[Abstract]
4. de Saint-Vis B, Vincent J, Vandenabeele S, Vanbervliet B, Pin JJ, it-Yahia S, Patel S, Mattei MG, Banchereau J, Zurawski S, et al. A novel lysosome-associated membrane glycoprotein, DC-LAMP, induced upon DC maturation, is transiently expressed in MHC class II compartment. Immunity 1998;9:325–336.[CrossRef][Medline]

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