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. Understanding the possible kinetic expression of vascular cell adhesion molecule-1 (VCAM-1) in the middle ear cavity during an inflammatory cascade in vivo may be important for clarifying local immunological responses in otitis media. Two inflammatory models were produced in the rat and involved acute middle ear mucosal and cutaneous inflammation induced after inoculation or intradermal injection of lipopolysaccharide (LPS). After intravenous injection of both I-125-labeled anti-VCAM-1 and I-131-labeled control monoclonal antibody (mAb), the kinetic expression of VCAM-1 in the middle ear and skin was assessed by local radionuclide uptake. The biodistribution of an I-125-labeled anti-VCAM-1 mAb as a potential detector of focal inflammation was examined in normal rats. Both inflammatory lesions were characterized by early and sustained (up to 24 h) expression of VCAM-1, with maximal expression at 4 h after LPS stimulation. The kinetics of VCAM-1 expression was similar among the middle ear mucosa or skin specimens studied and different stimulation methods. A similar biodistribution and clearance of radioactivity 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 response produced. Although VCAM-1 upregulation is a very early event in the inflammatory cascade, I-125-labeled anti-VCAM-1 mAb may be useful for the early detection of focal inflammation in the middle ear.