Search

The aim of this study was to examine glycoconjugate secretion in human airways with and without an epithelium. Glycoconjugate release in supernatants derived from human airways in vitro was determined using an ELISA assay with an anti-human mucin monoclonal antibody (MAb 3D3). This monoclonal antibody reacted strongly with Leb antigen but also recognized in vitro Lea and Ley determinents. In 11 of the 34 different lung samples (32%) studied the glycoconjugate levels were below the threshhold of detection for this assay. The mean basal secretion of glycoconjugates in human airways in vitro was 100 ±28 μg/g tissue (Period I; n=23 different lung samples). The amount of glycoconjugate measured in the medium derived from human isolated bronchial ring preparations did not change under control conditions during the course of the experimental procedure (Period I; 128 ± 46 μg/g tissue and Period II; 159 ± 48 μg/g tissue; n=13 paired lung samples). In the supernatants of airway preparations with an intact epithelium the amount of glycoconjugates detected was 90 ± 38 μg/g tissue (Period I; n=12 different lung samples) and removal of the epithelium did not alter this basal glycoconjugate release (94 ± 60 μg/g tissue: Period I, n=8 different lung samples). The absence of the epithelial layer was confirmed by histological evaluation. Methacholine (100 μM) induced a 10- and four-fold increase in glycoconjugate release from airways with and without an epithelium, respectively. In contrast, in preparations with an epithelium, LTD4 (10 μM) and anti-IgE (dilution: 1/1000) did not cause an increase of glycoconjugate release. The methacholine difference between airways with and without an epithelium was not significantly different (P>0.10). However, a treatment with atropine (100 μM) prevented the increase of glycoconjugate release in preparations with an epithelium. These data derived from a limited number of experiments suggest that the epithelium may not regulate the basal or stimulated release of glycoconjugates from isolated human airways.

Heman airway preparations at resting tone were relaxed with either the leukotriene synthesis inhibitor BAY x1005 (3 μM), chlorpheniramine (1 μM) or the thromboxane receptor antagonist BAY u3405 (0.1 μM). The response to anti-IgE (1:1000) was 58 ± 8% of acetylcholine pre-contraction (2.19 ± 0.28 g). Indomethacin (3 μM) enhanced the anti-IgE-induced contraction by 28%. The anti-IgE maximal response was not modified by either chlorpheniramine, BAY x1005 or BAY u3405. When the tissues were treated with either BAY xl005/indomethacin or BAY x1005/chlorpheniramine, the anti-IgE-induced contraction was reduced. In addition, in presence of BAY xl005/indomethacin/chlorpheniramine the response was completely blocked. These results suggest that mediatots released during anti-IgE challenge cause airway contraction which may mask the evaluation of the leukotriene component.