CC chemokines play an important role in the pathogenetic mechanisms of
interstitial lung disease, while a downregulation of
CC chemokine receptor (CCR)5 in the fibrotic stages of
sarcoidosis has been observed. To evaluate the involvement of
CC chemokines and the expression of CCR5 in
idiopathic pulmonary fibrosis (IPF) and, more specifically, in
usual interstitial pneumonia, 35 subjects were studied.
CC chemokine ligand (CCL)2, CCL3 and CCL4 levels were measured in the bronchoalveolar lavage fluid (BALF) of 18 nonsmoker control subjects and 17 patients affected by IPF. CCR5 expression was evaluated in alveolar macrophages and lymphocytes. The BALF levels of all
chemokines were significantly increased in IPF: median (range) CCL3 1.6 (1.0-11.1) versus 1.2 (0.0-3.8) pg x mL(-1); CCL4 6.2 (1.3-96.0) versus 3.4 (0.3-6.8) pg x mL(-1); and CCL2 60.1 (16.7-251.3) versus 4.6 (0.5-119.4) pg x mL(-1). CCL2 levels correlated negatively with the
carbon monoxide diffusing capacity of the lung (D(L,CO)) and arterial
oxygen tension. CCR5 expression was significantly reduced in lymphocytes from IPF compared with controls. The
CC chemokines investigated are involved in the inflammatory mechanisms of
idiopathic pulmonary fibrosis, and the results are in agreement with the hypothesis of a downregulation of the T-helper 1 immunological response in this disease.