PREVENTION OF PROTEINURIA BY THE ADMINISTRATION OF ANTI-INTERLEUKIN-8 ANTIBODY IN EXPERIMENTAL ACUTE IMMUNE COMPLEX-INDUCED GLOMERULONEPHRITIS

被引:137
作者
WADA, T
TOMOSUGI, N
NAITO, T
YOKOYAMA, H
KOBAYASHI, K
HARADA, A
MUKAIDA, N
MATSUSHIMA, K
机构
[1] KANAZAWA UNIV,SCH MED,DEPT INTERNAL MED 1,KANAZAWA,ISHIKAWA 920,JAPAN
[2] KANAZAWA UNIV,CANC RES INST,DEPT PHARMACOL,KANAZAWA,ISHIKAWA 920,JAPAN
关键词
D O I
10.1084/jem.180.3.1135
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Glomerular infiltration by neutrophils is a hallmark of acute glomerulonephritis. The pathophysiological role of interleukin 8 (IL-8), a potent neutrophil chemotactic cytokine (chemokine), was explored in an animal model of acute immune complex-mediated glomerulonephritis by administering a neutralizing antibody against IL-8. Repeated injection of bovine serum albumin (BSA) into rabbits caused the deposition of immune complexes consisting of BSA and rabbit IgG in glomeruli. Histological analyses revealed a small but significant number of neutrophils in glomeruli and the fusion of epithelial cell foot processes. Concomitantly, urinary levels of protein and albumin increased markedly(3.20 +/- 0.97 and 1.39 +/- 0.53 mg/h, respectively) compared with those of untreated animals (0.77 +/- 0.21 and 0.01 +/- 0.01 mg/h, respectively). Anti-IL-8 antibody treatment decreased the number of neutrophils in glomeruli by 40% and dramatically prevented the fusion of epithelial cell foot process Furthermore, treatment with anti-IL-8 antibody completely normalized the urinary levels of protein and albumin (0.89 +/- 0.15 and 0.02 +/- 0.01 mg/h, respectively). These results indicated that IL-8 participated in the impairment of renal functions in experimental acute immune complex-mediated glomerulonephritis through activating as well as recruiting neutrophils.
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页码:1135 / 1140
页数:6
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