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Compares the serum Clara cell 10-kDa protein (CC10) concentrations in healthy and asthmatic nonsmokers. Mutation of the CC10/human uteroglobin gene in patients with atopic asthma; Decrease in CC10-positive cells in the epithelial lining of bronchioles in smokers who had normal pulmonary function; Average serum CC10 levels in patient treated with oral and inhaled corticosteroid.

Examines the correlation between surfactant protein (SP)-A and clara cell 10-kDa protein (CC10) values in brochoalveolar lavage (BAL) fluids in healthy subjects using enzyme-linked immunosorbent assays. Similarities between clara cells and human urinary protein; Different components of the surfactant; Effect of cigarette smoking on SP-A and CC10 levels in BAL fluids.

Since tumor necrosis factor (TNF) is known to be involved in granuloma formation in sarcoidosis, and soluble TNF receptors (sTNF-Rs) inhibit TNF action in vivo, we evaluated the levels of sTNF-Rs in the bronchoalveolar lavage fluids (BALF) of 31 subjects using an enzyme-linked immunosorbent assay. Our group consisted of 13 patients with sarcoidosis (7 sarcoidosis patients who received no treatment and 6 who received corticosteroid therapy) and 18 control subjects (11 healthy nonsmokers and 7 asymptomatic smokers). Type II (75-kDa), but not type I (55 kDa) sTNF-R in BALF was elevated significantly in patients with sarcoidosis compared with the healthy nonsmokers (type I: 126.7 ± 17.6 pg/ml BALF vs 79.4 ± 16.5 pg/ml BALF, p > 0.05; type II: 98.3 ± 27.8 pg/ml BALF vs 26.7 ± 4.9 pg/ml BALF, p < 0.05). Although levels of type I sTNF-R in BALF from sarcoidosis patients were not correlated with any cellular profiles of BALF, concentrations of type II correlated significantly with the numbers of lymphocytes in BALF. We concluded that sTNF-R is a normal constituent of the epithelial lining fluids and that levels of type II sTNF-R are elevated significantly in the BALF from individuals with sarcoidosis. This suggests that sTNF-Rs may influence the local bioactivity of TNF and may also contribute to the pathogenesis of sarcoidosis. [ABSTRACT FROM AUTHOR]