Endothelial adhesion molecule expression is unaltered in the peripheral nerve from patients with AIDS and distal sensory polyneuropathy

• Published in: Journal of neuroimmunology Vol. 178; no. 1; pp. 111 - 116
• Main Authors: Fenzi, Flavio, Rossi, Francesca, Rava, Marta, Cavallaro, Tiziana, Ferrari, Sergio, Rizzuto, Nicolò
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.09.2006
• Subjects: Acquired Immunodeficiency Syndrome - complications; Adult; Blood vessels; Cell Adhesion Molecules - biosynthesis; Distal sensory polyneuropathy; Endothelial adhesion molecules; Endothelial Cells - metabolism; Female; HIV infection; Human immunodeficiency virus; Humans; Immunohistochemistry; Male; Middle Aged; Peripheral Nervous System Diseases - etiology; Peripheral Nervous System Diseases - metabolism; Sural nerve; Sural Nerve - blood supply; Sural Nerve - metabolism; Sural Nerve - pathology; Immunohistochemistry; Blood vessels; Endothelial adhesion molecules; Distal sensory polyneuropathy; HIV infection; Sural nerve
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/j.jneuroim.2006.06.013

Some evidence suggests that endothelial dysfunction, including altered expression of cell adhesion molecules contributes to pathophysiology of nervous system disorders in the course of HIV infection. In this immunohistochemical study we investigated and compared the expression of E-selectin, intercellular adhesion molecule-1 (ICAM-1), platelet endothelial cell adhesion molecule-1 (PECAM-1) in peripheral nerve blood vessels from patients with distal sensory polyneuropathy (DSP) and control patients with other axonal neuropathies. Similar quantitative pattern of immunoreactivity was found in patients with DSP and controls. E-selectin and PECAM-1 immunostained vessels tended to increase in number only in patients with major CD4 cell depletion. The vascular endothelium of the peripheral nerve in HIV-infected subjects with DSP shows no changes facilitating the migration of infected or activated monocytes/macrophages into the nerve. These phenomena probably do not play a critical role in the development of axonal damage in DSP.