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(Chest. 2006;130:982-988.)
© 2006 American College of Chest Physicians

Different Angiogenic Activity in Pulmonary Sarcoidosis and Idiopathic Pulmonary Fibrosis*

Katerina M. Antoniou, MD, PhD; Argyris Tzouvelekis, MD; Michael G. Alexandrakis, MD, PhD; Katerina Sfiridaki, MD; Ioanna Tsiligianni, MD, PhD; George Rachiotis, MD, PhD; Nikolaos Tzanakis, MD, PhD; Demosthenes Bouros, MD, PhD, FCCP; Joseph Milic-Emili, MD, PhD and Nikolaos M. Siafakas, MD, PhD, FCCP

* From the Departments of Thoracic Medicine (Drs. Antoniou, Tsiligianni, Tzanakis, and Siafakas) and Hematology (Dr. Alexandrakis), University of Crete, Heraklion, Greece; Department of Pneumonology (Drs. Tzouvelekis and Bouros), Democritus University of Thrace, Alexandroupolis, Greece; Department of Hematology (Dr. Sfiridaki), Venizeleion General Hospital, Heraklion, Greece; Department of Experimental Physiology (Dr. Rachiotis), University of Athens, Greece; and Department of Pneumonology (Dr. Milic-Emili), McGill University, Montreal, QC, Canada.

Correspondence to: Nikolaos M. Siafakas, MD, PhD, FCCP, Professor of Thoracic Medicine, Department of Thoracic Medicine, University Hospital, Medical School, University of Crete, Heraklion 71110 Crete, Greece; e-mail: siafak{at}med.uoc.gr

Abstract

Background: Recent evidence has shown that several chemokines—including those involved in angiogenesis—have been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and sarcoidosis. We speculated that these differences could be attributed to distinct angiogenic and angiostatic profiles. This hypothesis was investigated by estimating the levels of three angiogenic chemokines (growth-related gene [GRO]-{alpha}, epithelial neutrophil-activating protein [ENA]-78, and interleukin [IL]-8), and three angiostatic chemokines (monokine induced by interferon (IFN)-{gamma} [MIG], IFN-{gamma}–inducible protein [IP]-10, and IFN-{gamma}–inducible T-cell {alpha} chemoattractant) in serum and BAL fluid (BALF).

Methods: We studied prospectively 20 patients with sarcoidosis (median age, 46 years; range, 25 to 65 years), 20 patients with IPF (median age, 68 years; range, 40 to 75 years), and 10 normal subjects (median age, 39 years; range, 26 to 60 years).

Results: The GRO-a serum and BALF levels of IPF patients were found significantly increased in comparison with healthy subjects (799 pg/mL vs 294 pg/mL [p = 0.022] and 1,827 pg/mL vs 94 pg/mL [p < 0.001], respectively) and sarcoidosis patients (799 pg/mL vs 44 pg/mL [p < 0.001] and 1,827 pg/mL vs 214 pg/mL [p < 0.001], respectively). Moreover, ENA-78 and IL-8 BALF levels in IPF patients were significantly higher compared with sarcoidosis patients (191 pg/mL vs 30 pg/mL [p < 0.001] and 640 pg/mL vs 94 pg/mL [p = 0.03], respectively). MIG serum levels in IPF patients were found significantly upregulated in comparison with sarcoidosis patients and healthy control subjects. However, MIG and IP-10 BALF levels (1,136 pg/mL vs 66 pg/mL [p < 0.001] and 112 pg/mL vs 56 pg/mL [p = 0.037], respectively) were significantly higher in sarcoidosis patients compared with IPF patients.

Conclusions: Our data suggest distinct angiogenic profiles between IPF and sarcoidosis, indicating a potential different role of CXC chemokines in the local immunologic response in IPF and pulmonary sarcoidosis.

Key Words: angiogenesis • angiostasis • CXC chemokines • growth-related gene-{alpha} • interferon-{gamma}–inducible protein-10 • interferon-{gamma}–inducible T-cell {alpha} chemoattractant • monokine induced by interferon-{gamma}






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