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Airway dendritic cell phenotypes in inflammatory diseases of the human lung

¹ Dept of Pneumology, University of Rostock, Rostock, Germany. ² Both authors contributed equally to this article.

CORRESPONDENCE: M. Lommatzsch, Abteilung für Pneumologie, Klinik und Poliklinik für Innere Medizin, Universität Rostock, Ernst-Heydemann-Str. 6, 18057 Rostock, Germany. Fax: 49 3814947392. E-mail: marek.lommatzsch{at}med.uni-rostock.de

Keywords: Bronchoalveolar lavage fluid, dendritic cells, idiopathic pulmonary fibrosis, pneumonia, sarcoidosis

Received: March 26, 2007
Accepted June 27, 2007

Airway dendritic cells (DCs) are key regulators of pulmonary immune responses. However, information is limited regarding the characteristics of airway DCs in human lung diseases.

Plasmacytoid DCs (pDCs) and myeloid DCs (mDCs) were analysed using four-colour flow cytometry in bronchoalveolar lavage fluid (BALF) from nonsmoking controls and patients with sarcoidosis, idiopathic pulmonary fibrosis (IPF) and pneumonia (in the presence or absence of immunosuppression).

Compared with controls, immunocompetent patients with pneumonia displayed strongly enhanced pDC counts in BALF. In contrast, pDC counts in BALF from immunocompromised patients with pneumonia were even lower than in controls. This discrepancy was not explained by a different chemotactic milieu in the airways; all patients with pneumonia were characterised by strongly increased concentrations of the pDC-attracting chemokine, CXC chemokine ligand 10, in BALF. Patients with IPF were characterised by normal percentages of DC subtypes. However, the mDCs of patients with IPF were not as mature (CD83-positive) as those of controls. Patients with sarcoidosis displayed a unique increase in CD1a-negative mDCs in the airways. In addition, there was altered expression of costimulatory molecules (increased CD80 and decreased CD86 expression) on mDCs in patients with sarcoidosis.

These data suggest that inflammatory diseases of the human lung are associated with a differential phenotype and recruitment of airway dendritic cells.

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