Inflammation-induced modulation of cellular galectin-1 and-3 expression in a model of rat peritonitis

被引:43
|
作者
Gil, CD
Cooper, D
Rosignoli, G
Perretti, M
Oliani, SM
机构
[1] UNESP, Dept Biol, Inst Biociencias Letras & Ciencias Exatas, BR-15054000 Sao Jose Do Rio Preto, SP, Brazil
[2] FAMERP, Fac Med, Dept Agron, BR-15090000 Sao Jose Do Rio Preto, SP, Brazil
[3] Univ Fed Sao Paulo, Sao Paulo Sch Med, Postgrad Morphol, BR-04023900 Sao Paulo, Brazil
[4] Barts & London Queen Marys Sch Med & Dent, William Harvey Res Inst, London ECIM 6BQ, England
基金
巴西圣保罗研究基金会;
关键词
In vivo inflammation; mast cell; neutrophil; endothelial cell; macrophage;
D O I
10.1007/s00011-005-0059-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Objective and design: To investigate the effect of galectin-1 (Gal-1) and -3 (Gal-3) on leukocyte migration and analyze the expression of both galectins in inflammatory cells using a model of rat peritonitis. Material or Subjects: Sprague-Dawley rats (n = 4 per group). Treatment: Peritonitis was induced in animals through intraperitoneal injection of carrageenin (1.5 mg/kg) and rat mesenteries were analyzed at different time points (0, 4, 24 and 48h). For pharmacological treatment, rats received intravenous injection of Gal-1 or -3 (3 mu g/kg) followed by carrageenin. Methods: Western blotting and immunoelectron microscopy analysis. Statistical analysis was performed using ANOVA followed by Bonferroni test. Results: Pharmacological treatment with Gal-1, but not Gal-3, inhibited (similar to 50%) leukocyte recruitment into the peritoneal cavity at 4h time-point. In this early phase, immunogold staining of mesenteries showed a diminished Gal-3 expression in degranulated mast cells and Gal-1 in transmigrated neutrophils (similar to 20% reduction compared to intravascular cells). In the later phases (24 and 48 h), leukocyte turnover was associated with augmented Gal-1 expression in neutrophils and macrophages and Gal-3 in mast cells and macrophages. Conclusions: These results point to a balanced expression of cell-associated-Gal-1/Gal-3 and might impact on the development of new therapeutic strategies for inflammatory diseases.
引用
收藏
页码:99 / 107
页数:9
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