Effect of exogenous galectin-1 on leukocyte migration: modulation of cytokine levels and adhesion molecules

• Autor(a) principal: Gil, Cristiane Damas [UNIFESP]
• Data de Publicação: 2011
• Outros Autores: Gullo, Caio Eduardo, Oliani, Sonia Maria [UNIFESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNIFESP
• Texto Completo: http://www.ijcep.com/1012003A.html; http://repositorio.unifesp.br/handle/11600/44030
• topic: CD11b; CD62L; monocyte; neutrophil; zymosan peritonitis; immunocytochemistry

The effect of exogenous Gal-1 on cellular response and adhesion molecule expression was investigated in a classical model of acute inflammation induced by zymosan. C57BL6 mice, treated or not with human recombinant (hr) Gal-1, received i.p. injection of zymosan and peritoneal exudate, blood and mesentery were processed for cellular, biochemical, light and electron microscopic analysis after 4 and 24 h. Zymosan peritonitis provoked the expected signs of inflammation at 4 h, including a significant increase in extravasated PMNs in the mesentery and peritoneal exudate, mirrored by blood neutrophilia. These changes subsided after 24 h. Ultrastructural immunocytochemical analysis of PMNs showed significant Gal-1 expression and co-localization with L-selectin and beta 2-integrin in the plasma membrane and cytoplasm. Pharmacological treatment with hrGal-1 at 4 h produced an inhibition of PMN migration, associated with diminished expression of adhesion molecules, particularly beta 2-integrin, and TNF-alpha and IL1 beta release by peritoneal cells. At 24 h, Gal-1 induced an increase in mononuclear phagocytic cell recruitment. In conclusion, our data propose an important mechanism of anti-inflammatory action of Gal-1, initially by modulation of proinflammatory cytokine release and PMN migration through an imbalance between adhesion molecule expression and, later, by promoting monocyte-macrophage recruitment.