Clinical and histopathological progression of lesions in lupus-prone (NZB x NZW) F1 mice

被引:19
作者
Burnett, R [1 ]
Ravel, G
Descotes, J
机构
[1] MDS Pharma Serv, F-69210 St Germain En Laye, France
[2] Poison Ctr, F-69424 Lyon 03, France
[3] INSERM, U503, F-69424 Lyon 03, France
关键词
(NZB x NZW) F-1 mice; histopathology; kidney; liver; immunotoxicology; autoimmunity;
D O I
10.1016/j.etp.2004.04.010
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
This study was conducted to review the progression with age of renal and other changes in (NZB x NZW) F-1 females obtained from a commercial colony, housed under SPF conditions. Sixty-two mice were given food and water ad libitum and sacrificed at intervals up to 47 weeks of age. Routine haernatology and urinalysis were performed at reaular intervals. The serum levels of IgA, IgG, IgM and antinuclear antibody levels were monitored along with urinary protein. Major organs and tissues from all animals were preserved and examined. Special attention was paid to the kidneys: in addition to routine 4-mum paraffin sections, 1-mum resin sections were prepared and examined. Positive levels of urinary protein (> 1 g/L) were only found in 50% of the animals, even at 32 weeks of age. Histopathologically, the expected type of glomerular damage was present; but the incidence and severity of the change were low, with only 33% of the mice affected at 32 weeks of age. Most mice had fatty vacuolation in the liver. At 24 weeks of age, 50% of the mice sacrificed had haemorrhagic degeneration of the liver. This was not seen at later time points. Only two mice survived until 47 weeks of age. In Summary, these findings were of the expected type, but at a much lower incidence and severity than formerly reported. The background of the strain and the experimental conditions are of great importance in the progress of these renal lesions. The lack of homogeneity of the renal changes would make it difficult to determine any influence of xenobiotics on the progress of autoimmune diseases. (C) 2004 Elsevier GmbH. All rights reserved.
引用
收藏
页码:37 / 44
页数:8
相关论文
共 20 条
[1]   Genetic epidemiology - Systemic lupus erythematosus [J].
Ahmad, YA ;
Bruce, IN .
ARTHRITIS RESEARCH, 2001, 3 (06) :331-336
[2]   Mercury induces polyclonal B cell activation, autoantibody production and renal immune complex deposits in young (NZBxNZW)F1 hybrids [J].
AlBalaghi, S ;
Moller, E ;
Moller, G ;
AbediValugerdi, M .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1996, 26 (07) :1519-1526
[3]  
ALEXANDER NJ, 1987, AM J PATHOL, V127, P106
[4]  
BURNET FM, 1965, AUSTRALAS ANN MED, V14, P185
[5]  
CHOU ST, 1969, BRIT J EXP PATHOL, V50, P250
[6]   Dissection of the effects of tumor necrosis factor-α and class II gene polymorphisms within the MHC on murine systemic lupus erythematosus (SLE) [J].
Fujimura, T ;
Hirose, S ;
Jiang, Y ;
Kodera, S ;
Ohmuro, H ;
Zhang, DQ ;
Hamano, Y ;
Ishida, H ;
Furukawa, S ;
Shirai, T .
INTERNATIONAL IMMUNOLOGY, 1998, 10 (10) :1467-1472
[7]  
GAMBLE CN, 1975, AM J CLIN PATHOL, V63, P310
[8]  
HEYLER BJ, 1963, NATURE, V197, P197
[9]   RENAL LESIONS IN AUTO-IMMUNE MOUSE STRAINS NZB AND FI NZBXNZW [J].
HICKS, JD ;
BURNET, FM .
JOURNAL OF PATHOLOGY AND BACTERIOLOGY, 1966, 91 (02) :467-&
[10]  
Howie J B, 1968, Adv Immunol, V9, P215, DOI 10.1016/S0065-2776(08)60444-7