Open AccessExpression of Interleukin‐16 in Sciatic Nerves, Spinal Roots and Spinal Cords of Experimental Autoimmune Neuritis Rats
Author(s) -
Zhang ZhiYuan,
Zhang Zhiren,
Fauser Uwe,
Schluesener Hermann J.
Publication year - 2009
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2008.00172.x
Subject(s) - neuritis , medicine , sciatic nerve , spinal cord , pathological , peripheral nervous system , pathology , central nervous system , anatomy , surgery , psychiatry
Experimental autoimmune neuritis (EAN) is a well‐known animal model of Guillain‐Barré Syndrome. In this study, we studied the spatiotemporal expression of interleukin‐16 (IL‐16) in the nervous system of EAN rats and pharmacological effects of minocycline on IL‐16 expressions in EAN rats. In sciatic nerves and dorsal/ventral roots of EAN rats, IL‐16 + cells, identified as macrophages and T cells, were mainly found to concentrate around blood vessels. However, in spinal cords, IL‐16 + microglial cells were mainly found in lumbar dorsal horns. Massive IL‐16 + cell accumulation in sciatic nerves and spinal roots was temporally correlated with severity of neurological signs of EAN. Furthermore, a strong correlation of IL‐16 + cell accumulation with local demyelination in perivascular areas of sciatic nerves, and significant reduction of IL‐16 + cell numbers in sciatic nerves and spinal cords by minocycline suggested a pathological contribution of IL‐16 + cells in EAN. Taken together, robust IL‐16 + cell accumulation in the nervous system and its temporal correlation with severity of neurological signs in EAN might suggest a pathological role of IL‐16 in EAN, which makes IL‐16 a potential pharmacological target.