Open AccessDifferential Macrophage/Microglia Activation in Neocortical EAE Lesions in the Marmoset Monkey
Author(s) -
Merkler Doron,
Böscke Robert,
Schmelting Barthel,
Czéh Boldizsár,
Fuchs Eberhard,
Brück Wolfgang,
Stadelmann Christine
Publication year - 2006
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.1750-3639.2006.00004.x
Subject(s) - marmoset , microglia , white matter , pathology , neocortex , multiple sclerosis , myelin , cerebral cortex , experimental autoimmune encephalomyelitis , biology , encephalomyelitis , callithrix , myelin oligodendrocyte glycoprotein , lesion , neuroscience , medicine , inflammation , central nervous system , immunology , magnetic resonance imaging , paleontology , radiology
Recent studies revealed an important involvement of the cerebral cortex in multiple sclerosis (MS) patients. Cortical lesions in MS were reported to be less inflammatory and to show less structural damage than white matter lesions. Animal models reflecting the histopathological hallmarks of cortical demyelinated lesions in MS are sparse. Induction of experimental autoimmune encephalomyelitis (EAE) in the common marmoset has turned out to be an attractive non‐human‐primate model for MS. In the present study we investigated the presence and detailed cellular composition of cortical inflammatory demyelinating pathology in the common marmoset upon immunization with myelin oligodendrocyte glycoprotein (MOG). Extensive cortical demyelination reflecting the topographically distinct cortical lesion types in MS patients was revealed by immunohistochemistry for myelin basic protein (MBP). We explored the density of T‐ and B‐lymphocytes, MHC‐II expressing macrophages/microglia cells and early activated macrophages (MRP14) at perivascular and parenchymal lesions sites in neocortex and subcortical white matter. Despite a similar density of perivascular inflammatory infiltrates in the demyelinated neocortex, a considerable lower fraction of macrophages was found to express MRP14 in the neocortex indicating a different activation pattern in cortical compared with white matter lesions. Furthermore, cortical EAE lesions in marmoset monkeys revealed immunoglobulin leakage and complement component C9 deposition in intracortical but not subpial demyelination. Our findings indicate that the inflammatory response, especially macrophage and microglia activation, may be regulated differently in gray matter areas in primate brain.