EXPRESSION PROFILE OF VASCULAR CELL-ADHESION MOLECULE-1 (CD106) IN THE MIDDLE-EAR USING RADIOLABELED MONOCLONAL-ANTIBODY

Adhesive interactions between leukocytes and endothelium are required for subsequent leukocyte extravasation toward inflammatory sites. Unde rstanding the possible kinetic expression of vascular cell adhesion mo lecule-1 (VCAM-1) in the middle ear cavity during an inflammatory casc ade in vivo may be important for clarifying local immunological respon ses in otitis media. Two inflammatory models were produced in the rat and involved acute middle ear mucosal and cutaneous inflammation induc ed after inoculation or intradermal injection of lipopolysaccharide (L PS). After intravenous injection of both I-125-labeled anti-VCAM-1 and I-131-labeled control monoclonal antibody (mAb), the kinetic expressi on of VCAM-1 in the middle ear and skin was assessed by local radionuc lide uptake. The biodistribution of an I-125-labeled anti-VCAM-1 mAb a s a potential detector of focal inflammation was examined in normal ra ts. Both inflammatory lesions were characterized by early and sustaine d (up to 24 h) expression of VCAM-1, with maximal expression at 4 h af ter LPS stimulation. The kinetics of VCAM-1 expression was similar amo ng the middle ear mucosa or skin specimens studied and different stimu lation methods. A similar biodistribution and clearance of radioactivi ty between I-125-labeled anti-VCAM-1 mAb and I-131- Or Tc-99m-labeled control mAb were observed. The present results suggest that functional VCAM-1 induced by LPS is expressed in both middle ear tissue and skin lesions and may Flay a role in the initial stage of inflammatory resp onse produced. Although VCAM-1 upregulation is a very early event in t he inflammatory cascade, I-125-labeled anti-VCAM-1 mAb may be useful f or the early detection of focal inflammation in the middle ear.