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
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.