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Published online before print April 12, 2006
Eur Respir J 2006, doi:10.1183/09031936.06.00116205
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ORIGINAL ARTICLE

High ICAM-1 gene expression in pulmonary fibroblasts of COPD patients: a reflection of an enhanced immunological function

A. Zandvoort 1, Y.M. van der Geld 2, M.R. Jonker 1, J.A. Noordhoek 3, J.T.W.M. Vos 2, Jelle Wesseling 2, Henk F Kauffman 4, Wim Timens 2, Dirkje S Postma 3

1 Depts of Pathology and Laboratory Medicine; and Pulmonology
2 Depts of Pathology and Laboratory Medicine
3 Pulmonology
4 Allergology, University Medical Center Groningen, University of Groningen, The Netherlands


  Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by destruction of extracellular matrix (ECM) in parenchymal areas, whereas the bronchial walls can show fibrosis. In addition, an extensive inflammatory process is observed. CD8+ T cells, located throughout the lung, and epithelial cells in centrally located airways produce cytokines involved in the inflammatory process. These cytokines may influence the present fibroblasts, the key effectors in the defective ECM repair and maintenance in COPD.

We explored the effects of the cytokine microenvironment on cell-cell interaction gene expression in pulmonary fibroblasts of controls (n=6), GOLD stage II (n=7) and stage IV (n=7) COPD patients. We simulated the in vivo microenvironment using supernatants of CD3/CD28 stimulated CD8+ T cells isolated from peripheral blood of COPD patients, supernatant of a bronchial epithelial cell line, or a combination of both.

Our data shows that fibroblasts of COPD patients display an altered response to the cytokine microenvironment, depending on both the disease stage and the central or peripheral location in the lung. Especially adhesion related genes are upregulated in fibroblasts of COPD patients, which can indicate a more pronounced role of fibroblasts in the inflammatory process in COPD, possibly resulting in reduced function as effectors of ECM repair.

Keywords:  CD8+ T cells, chronic inflammation, COPD, ICAM-1, lung fibroblasts




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