Expression of the CD11/CD18 cell surface adhesion glycoprotein family and MHC class II antigen on blood monocytes and alveolar macrophages in interstitial lung diseases

Abstract

The expression of molecules of the CD11/CD18 cell surface adhesion glycoprotein family and HLA/DR antigen was studied on peripheral blood monocytes (PBM) and alveolar macrophages (AM) in bronchoalveolar lavage (BAL) fluid from patients with sarcoidosis, idiopathic pulmonary fibrosis (IPF), and extrinsic allergic alveolitis (EAA). Patients with these interstitial lung diseases showed increased numbers of macrophages in BAL fluid. This was probably caused by an increased influx of PBM to the alveoli since the numbers of cells with a monocytic morphology were also significantly increased in BAL samples from patients with interstitial lung disease, most prominently in IPF and EAA. The increased influx of PBM into the alveoli in patients with interstitial lung diseases was not reflected by an increased expression of the CD11/CD18 leukocyte function antigens on PBM. In healthy volunteers as well as in those with sarcoidosis, IPF, and EAA, the percentages of AM positive for CD11b (the C3bi complement receptor) and CD11c were lower than among PBM. This indicates that the expression of these cell surface adhesion molecules is downregulated during maturation and migration of PBM to the alveoli. The absolute numbers of AM positive for CD11b were increased in BAL fluid of IPF and EAA patients compared to healthy volunteers. EAA patients also showed increased absolute numbers of AM positive for CD11a and CD11c. This differentially increased expression of these leukocyte function antigens on AM suggests the influence of locally produced cytokines.

Chronic smoke exposure alters the phenotype pattern and the metabolic response in human alveolar macrophages

“…The receptors of the CD11/CD18 family and CD54 have been reported to be increased [20,29,30] on AM from patients with these disorders. Having the results from the present study in mind, one may speculate that smokers' AM spend a relatively shorter period being an effective antigen-presenting cell and have more phagocytic properties.…”

Characterization and quantification of alveolar monocyte-like cells in human chronic inflammatory lung disease

“…An elevated expression of monocyte-lineage surface antigens was found on AMs from patients with sarcoidosis [13,14,17,[35][36][37][38], idiopathic pulmonary fibrosis [15,16,[36][37][38], extrinsic allergic alveolitis [36,37], bronchogenic carcinoma [35], asthma [39], human immunodeficiency virus (HIV) infection [40], as well as in smoking individuals [41,42]. The increased expression of binding sites for several lectins by AMs from patients with interstitial lung disease may reflect the influx of immature blood monocytes and/or the emergence of a proinflammatory macrophage phenotype [43].…”

“…CD11b is the α-chain of a β 2 -integrin that is expressed at high levels on blood monocytes [36], quantitatively upregulated on the surface of fresh extravasated monocytes [45], and expressed at only low levels on mature AMs [35]. CD14 is a receptor for LPS that is expressed at high levels in normal blood monocytes, and at low levels in the subset of CD14+/CD16+ monocytes, as well as in mature AMs [46,47].…”

From granuloma to fibrosis in interstitial lung diseases: molecular and cellular interactions

“…Cellular adhesion molecules participate in the localization of macrophages and in antigen presentation by them [46], and increased expression of CD11b and CD54 by alveolar macrophages has been observed in sarcoidosis [46,47], and hypersensitivity pneumonitis [48]. Another potential mediator is basic fibroblast growth factor (bFGF), which is known to modify cell adhesion properties [49], and is produced by macrophages.…”