Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats
| Autor: | Yoshinori Tsuchiyama, Masahiro Yamamura, Jun Wada, Kenichi Shikata, Kazuyuki Hida, Hong Zhang, Keita Hiragushi, Yashpal S. Kanwar, Yoshitaka Morita, Hirofumi Makino |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
CD8+ cells Galectin 1 Lymphocyte Galectin 3 Galectins T-Lymphocytes Kidney Glomerulus Apoptosis Biology Kidney Rats Inbred WKY immune response Antibodies Dexamethasone Immune system Adjuvants Immunologic Internal medicine Lectins otorhinolaryngologic diseases medicine Macrophage Animals Glucocorticoids Galectin Autoantibodies Nephritis urogenital system Immune Sera Antigens Differentiation macrophages Rats Proteinuria crescentic glomerulonephritis Endocrinology medicine.anatomical_structure Hemagglutinins Nephrology Galectin-3 Galectin-1 Female Spleen |
| Zdroj: | ResearcherID |
| ISSN: | 0085-2538 |
| Popis: | Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats. Background Galectins are characterized by specific affinity for β-galactoside sugars, and they play a role in diverse biological processes, including cell adhesion, cell proliferation, and apoptosis. Galectin-1, -3, and -9 have been implicated in modulating the immune response. Methods Nephrotoxic serum nephritis, which is characterized by crescent formation and glomerular influx of CD8 + cells into glomerular capillaries, was induced in Wistar Kyoto (WKY) rats by injecting rabbit antiglomerular basement membrane serum. Following induction, the rats were treated either with phosphate-buffered saline or dexamethasone, galectin-1, galectin-3, or galectin-9 on alternate days and were sacrificed at day 14. At day 8, splenic lymphocytes were isolated and employed for terminal deoxytransferase-mediated uridine triphosphate nick end-labeling (TUNEL) assay to assess the degree of apoptosis, and the kidneys were utilized to determine the extent of influx of CD4 + and CD8 + cells and glomerular damage. Results Dexamethasone induced a marked apoptosis of splenic CD4 + and CD8 + cells, and it inhibited the production of anti-rabbit IgG and the influx of CD8 + cells and macrophages into the renal glomeruli. Crescent formation and excretion of urinary proteins were also reduced. Galectin-9 failed to induce apoptosis in the CD4 + cells; however, it induced apoptosis in the CD8 + cells and inhibited the infiltration of CD8 + cells. Although galectin-1 and -3 did not induce the apoptosis in the T cells, they inhibited the accumulation of macrophages in the renal glomeruli. Like dexamethasone, the galectins also reduced the crescentic formation, proliferation of glomerular cells, and excretion of urinary proteins. Conclusions Galectin-9 selectively induces apoptosis of the activated CD8 + cells, while the macrophage influx into the kidney is modulated by all three galectins. This finding raises an interesting possibility for the utility of galectins in the modulation of macrophages that are involved in immune-mediated glomerular diseases. |
| Databáze: | OpenAIRE |
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