Lymphocyte infiltrate is a hallmark of inflammatory responses. We have previously shown that de novo-induced endothelial
sialyl Lewis x (sLex) expression guides lymphocytes in an
L-selectin-dependent manner to sites of acute organ transplant rejections. In this research, we have analyzed five groups of chronic
lung inflammations to determine the presence of properly glycosylated, i.e., sulfated, sLex-decorated,
L-selectin ligands. Two anti-sLex (2F3 and HECA-452) and one anti-6- and/or 6'-sulfated and/or 6,6'-bisulfated (MECA-79)
monoclonal antibodies (mAbs) were used. The control lung specimens did not express
L-selectin ligands on endothelium. In contrast, the endothelial staining intensity and the number of positive peribronchial venules and capillaries with mAbs 2F3, HECA-452, and MECA-79 were significantly greater in bronchial biopsies from patients with
asthma compared with normal specimens (P<0.003). However, no significant increase of peribronchial endothelial reactivity with these
antibodies was observed in
adult respiratory distress syndrome,
chronic bronchitis,
fibrosing alveolitis, and granulomatous
inflammation compared with controls. These data suggest that sulfated sLex
glycans, acting putatively as
ligands for
L-selectin, could be instrumental in lymphocyte extravasation into human peribronchial lung tissue during
asthma, but not so important in several other inflammatory
lung diseases.