Glucocorticoid-induced differential expression of the sialylated and nonsialylated Lewis(a) epitopes and respective binding sites in human nasal polyps maintained under ex vivo tissue culture conditions.
We characterized the anti-inflammatory effects of budesonide on the expression of adhesion molecules involving Lewis(a) (Le(a)) epitope, its sialylated derivative (sLe(a)), and their respective binding sites in human nasal polyposis. By computer-assisted microscopy, we quantitatively characterized the level of histochemical expression of L- and P-selectins, sialylated and nonsialylated Le(a) epitopes, and their respective binding sites in both surface epithelium and glandular epithelium of human nasal polyps obtained from surgical resection, maintained under ex vivo tissue culture conditions for 24 hours, and treated or not with budesonide. Intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) were chosen as methodological controls, because data already published in the literature clearly indicated budesonide-mediated effects on ICAM-1 and VCAM-1 levels of expression. The present data show that budesonide significantly modified the levels of expression of ICAM-1 and VCAM-1, and to a lesser extent that of P-selectin, in the surface and glandular epithelia. Budesonide markedly decreased the levels of expression of the binding sites for both Le(a) and sLe(a), while those of Le(a) and sLe(a) remained globally unchanged. In conclusion, the present study documents that glucocorticoid-induced effects can encompass receptors for Le(a) epitopes different from E- and P-selectins on epithelial cells of human nasal polyps.
Delbrouck
Carine
C
Department of Otorhinolaryngology, Erasmus University Hospital, Brussels, Belgium.
Kaltner
Herbert
H
Danguy
André
A
Nifant'ev
Nikolay E
NE
Bovin
Nicolai V
NV
Vandenhoven
Guy
G
Gabius
Hans-Joachim
HJ
Kiss
Robert
R
Hassid
Sergio
S
D000893:Anti-Inflammatory Agents / Q000276:immunology* / Q000494:pharmacology; D001666:Binding Sites, Antibody / Q000187:drug effects; D019819:Budesonide / Q000276:immunology* / Q000494:pharmacology; D018395:CA-19-9 Antigen; D046508:Culture Techniques; D004353:Drug Evaluation, Preclinical; D019040:E-Selectin / Q000032:analysis / Q000187:drug effects*; D004804:Eosinophils / Q000276:immunology; D000939:Epitopes; D005732:Gangliosides / Q000032:analysis / Q000276:immunology*; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000276:immunology*; D006801:Humans; D006967:Hypersensitivity / Q000150:complications / Q000175:diagnosis; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000187:drug effects; D007983:Lewis Blood Group Antigens / Q000032:analysis / Q000276:immunology*; D009298:Nasal Polyps / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D019007:P-Selectin / Q000032:analysis / Q000187:drug effects*; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000187:drug effects
D000893:Anti-Inflammatory Agents; D018395:CA-19-9 Antigen; D019040:E-Selectin; D000939:Epitopes; D005732:Gangliosides; D007983:Lewis Blood Group Antigens; D019007:P-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019819:Budesonide; C064564:sialyl Le(a) ganglioside