Changes in the expression pattern of blood-brain barrier-associated pericytic aminopeptidase N (pAP N) in the course of acute experimental autoimmune encephalomyelitis.
The role of cerebral pericytes in blood-brain barrier (BBB) mechanisms is still a matter of controversy. Because acute experimental autoimmune encephalomyelitis (EAE) is characterized by a transient and focal perturbation of the BBB, we have utilized the model of adoptive transfer EAE to correlate the expression of the pericytic aminopeptidase N (pAP N) with the acute functional state of the BBB. We demonstrate that a significant downregulation of microvascular pAP N expression occurs, and the observed perturbation of the enzymatic BBB complement seems to be a sustained effect which persists even after recovery from clinical disease. At the peak of clinical disease, numerous pAP N expressing invasive cells were detected in white matter of the lumbar spinal cord. Through the use of a panel of different immunocytochemical markers these pAP N-immunopositive cells were characterized as ED 1-positive, most likely hematogenous macrophages. Activated resident microglial cells participate in the EAE-induced inflammatory process to only a minor extent.
Kunz
J
J
Institute of Anatomy, University of Regensburg, Germany.
Krause
D
D
Gehrmann
J
J
Dermietzel
R
R
D000208:Acute Disease; D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000201:enzymology*; D018826:CD13 Antigens / Q000032:analysis*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000201:enzymology*; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007150:Immunohistochemistry; D008833:Microcirculation / Q000201:enzymology; D051381:Rats; D011917:Rats, Inbred Lew; D013116:Spinal Cord / Q000201:enzymology*
D000949:Histocompatibility Antigens Class II; D018826:CD13 Antigens