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Chemokine/Cytokine Cocktail in Idiopathic Pulmonary Fibrosis

Department of Clinical and Experimental Medicine, Clinical Immunology and Hematology Branches, Padua University School of Medicine, Padua, Italy

Correspondence and requests for reprints should be addressed to Carlo Agostini, M.D., Dipartimento di Medicina Clinica e Sperimentale, Università di Padova, Immunologia Clinica and Ematologia, Via Giustiniani 2, 35128 Padova, Italy. E-mail: carlo.agostini{at}unipd.it

ABSTRACT

Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible fibrosing lung disease of unknown etiology and with an unfavorable outcome, leading ultimately to death due to respiratory failure. To date, no treatment strategies have been effective in modifying the natural course of IPF and its fatal outcome. The aberrant parenchymal remodeling is characterized by the expansion of fibroblasts/myofibroblasts, which form characteristic subepithelial foci, and by the abnormal deposition of extracellular matrix in the lung parenchyma. Although the pathophysiology underlying this disease has not yet been fully elucidated, animal models of pulmonary fibrosis have provided contributions in dissecting the molecular basis of this disease, focusing on the role of cytokines and chemokines as important pathogenetic mediators of lung fibrosis. Starting with the data obtained from animal models, this article provides a comment on a number of findings that suggest the possible role of the chemokine/cytokine system in the pathogenesis of IPF.

Key Words: idiopathic pulmonary fibrosis • cytokine • chemokine • bleomycin

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