title: Absence of PAF receptor alters cellular infiltrate but not rolling and adhesion of leukocytes in experimental autoimmune encephalomyelitis.
abstract: Experimental autoimmune encephalomyelitis (EAE) is a condition induced in some susceptible species to the study of multiple sclerosis (MS). The platelet activating factor (PAF) is an important mediator of immune responses and seems to be involved in MS. However, the participation of PAF in EAE and MS remains controversial. Thus, in this study, we aimed to evaluate the role of PAF receptor in the pathogenesis of EAE. EAE was induced using an emulsion containing MOG(35-55). EAE-induced PAF receptor knock out (PAFR(-/-)) mice presented milder disease when compared to C57BL/6 wild type (WT) animals. PAFR(-/-) animals had lower inflammatory infiltrates in central nervous system (CNS) tissue when compared to WT mice. However, intravital microscopy in cerebral microvasculature revealed similar levels of rolling and adhering leukocytes in both WT and PAFR(-/-) mice. Interleukine (IL)-17 and chemokines C-C motif legends (CCL)2 and CCL5 were significantly lower in PAFR(-/-) mice when compared to WT mice. Brain infiltrating cluster of differentiation (CD)4(+) leukocytes and IL-17(+) leukocytes was diminished in PAFR(-/-) when compared to WT mice. Taken together, our results suggest that PAF receptor is important in the induction and development of EAE, although it has no influence in rolling and adhesion steps of cell recruitment. The absence of PAF receptor results in milder disease by altering the type of inflammatory mediators and cells that are present in CNS tissue.
authors.affiliation: Laboratory of Immunopharmacology, Federal University of Minas Gerais, Belo Horizonte, Brazil. dhenrodrigues@gmail.com
authors.forename: David Henrique
authors.initials: DH
authors.lastname: Rodrigues
authors.forename: Norinne
authors.initials: N
authors.lastname: Lacerda-Queiroz
authors.forename: Aline Silva
authors.initials: AS
authors.lastname: de Miranda
authors.forename: Caio Tavares
authors.initials: CT
authors.lastname: Fagundes
authors.forename: Roberta Dayrell de Lima
authors.initials: RD
authors.lastname: Campos
authors.forename: Rosa Esteves
authors.initials: RE
authors.lastname: Arantes
authors.forename: Márcia de Carvalho
authors.initials: Mde C
authors.lastname: Vilela
authors.forename: Milene Alvarenga
authors.initials: MA
authors.lastname: Rachid
authors.forename: Mauro Martins
authors.initials: MM
authors.lastname: Teixeira
authors.forename: Antônio Lúcio
authors.initials: AL
authors.lastname: Teixeira
mesh_terms: D000818:Animals; D002448:Cell Adhesion / Q000276:immunology; D002454:Cell Differentiation / Q000502:physiology; D002490:Central Nervous System / Q000378:metabolism / Q000473:pathology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D018836:Inflammation Mediators / Q000378:metabolism / Q000502:physiology*; D007962:Leukocytes / Q000378:metabolism* / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010980:Platelet Membrane Glycoproteins / Q000172:deficiency* / Q000235:genetics / Q000502:physiology; D043562:Receptors, G-Protein-Coupled / Q000172:deficiency* / Q000235:genetics / Q000502:physiology
chemical_list: D018836:Inflammation Mediators; D010980:Platelet Membrane Glycoproteins; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor