Extensive surface phenotyping of alveolar macrophages in interstitial lungdisease

There is increasing evidence implicating activated macrophages in the patho genesis of interstitial and other lung diseases. We investigated whether th ere was a unique pattern of cell surface expression that constituted a dise ase-specific phenotype on alveolar macrophages from patients with interstit ial lung disease (ILD). Macrophage cell surface receptor expression of 19 s elected markers was assessed by indirect immunofluorescence and flow cytome try in bronchoalveolar lavage (BAL) fluids from patients with idiopathic pu lmonary fibrosis (IPF, n = 4), scleroderma (SCL-ILD, n = 14), mild asthma ( n = 7), allergy without asthma (n = 2), and normal subjects (n = 9). There was increased expression of adhesion receptors (CD11c, CD29, CD36, CD44, CD 49e, CD54), receptors involved in signal transduction and/or inflammation ( CD13, CD45, CD53), and other markers (CD9, CD52, CD71, CD98, HLA Class I) o n macrophages from ILD patients compared to the non-ILD group. Most markers upregulated on macrophages in ILD were significantly inversely correlated with clinical parameters of disease activity such as FEV1, FVC, and DLCO an d positively correlated with numbers of BAL neutrophils and eosinophils. In creased expression of several cell surface markers suggests that activated alveolar macrophages may contribute to the pathophysiology of IPF and SCL-I LD. (C) 2000 Academic Press.