SHED SOLUBLE ICAM-1 MOLECULES IN BRONCHOALVEOLAR LAVAGE CELL SUPERNATANTS AND SERUM OF PATIENTS WITH PULMONARY SARCOIDOSIS

Citation
I. Baumer et al., SHED SOLUBLE ICAM-1 MOLECULES IN BRONCHOALVEOLAR LAVAGE CELL SUPERNATANTS AND SERUM OF PATIENTS WITH PULMONARY SARCOIDOSIS, Lung, 175(2), 1997, pp. 105-116
Citations number
42
Categorie Soggetti
Respiratory System
Journal title
LungACNP
ISSN journal
03412040
Volume
175
Issue
2
Year of publication
1997
Pages
105 - 116
Database
ISI
SICI code
0341-2040(1997)175:2<105:SSIMIB>2.0.ZU;2-D
Abstract
The soluble form of intercellular adhesion molecule-1 (sICAM-1) might be a serum parameter of inflammatory activity gauging cellular interac tions with possible relevance in sarcoidosis. To address this question we measured sICAM-1 by enzyme-linked immunosorbent assay in serum and shedding of this molecule by bronchoalveolar lavage (BAL) cells in sa rcoidosis patients (44 and 40, respectively) and in controls (10 and 1 9, respectively). Serum concentrations of sICAM-1 (588.3 +/- 72.2 ng/m l) and its spontaneous release by BAL cells (9.9 +/- 1.5 ng/ml) in pat ients with active sarcoidosis were significantly higher than in those with inactive disease or controls, although no correlation was observe d. Significant correlations of sICAM-1 shedding by nonstimulated BAL c ells with the serum level of neopterin and of shedding by lipopolysacc haride-stimulated BAL cells with percentage of alveolar macrophages we re observed in active sarcoidosis. Kinetic cell culture experiments wi th peripheral blood mononuclears disclosed a rapid up-regulation of sI CAM-1 shedding and tumor necrosis factor-alpha release; however, at 5 h after stimulation a dissociation of their releases was observed. sIC AM-1 release was maintained over 2 days, whereas tumor necrosis factor -alpha release peaked at 5 and ceased after 43 h. These results provid e evidence that circulating and BAL cell culture-derived sICAM-1 refle ct the stage of sarcoid inflammation. Although sICAM-1 in BAL cell sup ernatants originates from alveolar macrophages; the absence of a corre lation with serum sICAM-1 concentration indicates that other cells are additional sources of the circulating pool of this molecule.