Resposta inflamatória induzida pela lectina de sementes de Dioclea rostrata: mecanismos e mediadores envolvidos.

• Autor(a) principal: Figueiredo, Jozi Godoy
• Data de Publicação: 2007
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Ceará (UFC)
• dARK ID: ark:/83112/0013000022x4v
• Texto Completo: http://www.repositorio.ufc.br/handle/riufc/18248
• topic: Bioquímica; Citocinas; Mediadores inflamatórios; Inflamação; Lectina; Macrófagos; Cytokines; Inflammatory mediators; Inflammation; Lectins; Macrophage; Lectina de sementes; Migração de neutrófilos

Lectins are proteins possessing a carbohidate moiety that are able to interact with biological systems eliciting a variety of effects. Vegetal lectins have been used as tools in the study of inflammation due to its ability to recognize carbohydrate residues in inflammatory cell membranes by means of its lectin domain. The present work studied the pro-inflammatory effects of the lectin from Dioclea rostrata seeds (Dros), a binder of α-methyl-D-manoside, on neutrophil migration ( NM ) [(in vivo and in vitro)]. The models of peritonitis, paw edema, and subcutaneous air pouch (in vivo), neutrophil chemotaxy and macrophage culture (in vitro) were utilized. It was found that Dros showed a pro-inflammatory activity in all of the above models. The increase in the number of macrophages by the pre-treatment of the animals with thioglycolate potentialized the Dros-induced NM. Also, the depletion of mast cells by the use of the substance 48/80 did not interfere in the lectin-induced NM. The above data suggest the involvement of macrophages but not mast cells in the mechanisms studied. The pre-treatment of the peritoneum with anti-inflammatory drugs like indomethacine, dexamethasone and thalidomide inhibited the NM. Dros induced chemotaxy in vitro and stimulated the synthesis / release of cytokines as TNF-α and IL-1 in addition to IL-10 and this way he/she suggests himself that more detailed studies are accomplished in continuities to this work to verify this lectin can be used in imunosupression models. In the paw edema model the lectin promoted an intense edema and a significant increase in the mieloperoxidase activity (when compared to the control group). The α-methyl-D-manoside reversted the Dros-induced NM and so it seems that Dros triggers the inflammatory response by means of the interaction of its lectin domain with sugars in the macrophage membrane. The present data suggest that Dros could be used as tools in biochemical and pharmacological studies.