Platelet-activating factor antagonists do not protect against the development of experimental autoimmune encephalomyelitis.
There is evidence suggesting the involvement of the platelet-activating factor (PAF) in central nervous system (CNS) functions. The possibility exists that PAF may be relevant in eliciting cell-mediated autoimmune phenomena in CNS. To assess the role of PAF in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), male Lewis rats were primed with whole spinal cord from guinea pig, emulsified in Freund's adjuvant supplemented with 10 mg/ml of Mycobacterium tuberculosis, H37Ra strain. Treatment with two different PAF antagonists (PCA 4248, WEB 2170) was applied starting from day 1 or day 5 postinoculation on a twice-daily basis. Neither PCA 4248 nor WEB 2170 suppressed the clinical signs of EAE. PAF concentration was measured in CNS tissue from the 9th day after inoculation to the 15th day, and no differences were found between control and EAE animals. These results suggest that PAF is not involved in the mediation of EAE.
Vela
L
L
Servicio de Neurología, Clínica Puerta de Hierro, Madrid, Spain.
García Merino
A
A
Fernández-Gallardo
S
S
Sánchez Crespo
M
M
López Lozano
J J
JJ
Saus
C
C
D000818:Animals; D001923:Brain Chemistry; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D010972:Platelet Activating Factor / Q000032:analysis / Q000037:antagonists & inhibitors* / Q000502:physiology; D051381:Rats; D011917:Rats, Inbred Lew
D010972:Platelet Activating Factor