OXYGEN RADICAL PRODUCTION IS INCREASED IN MACROPHAGES FROM DIABETES-PRONE BB-RATS

被引：26

作者：

BRENNER, HH ^{[1
]}

BURKART, V ^{[1
]}

ROTHE, H ^{[1
]}

KOLB, H ^{[1
]}

机构：

[1] UNIV DUSSELDORF,DIABET RES INST,HENNEKAMP 65,D-40225 DUSSELDORF,GERMANY

来源：

AUTOIMMUNITY | 1993年 / 15卷 / 02期

关键词：

AUTOIMMUNITY; OXYGEN RADICALS; MACROPHAGES; BB-RAT; DIABETES;

D O I：

10.3109/08916939309043883

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Macrophages from autoimmune diabetes prone BB rats were found to produce radical oxygen intermediates (ROI) at an enhanced rate when compared to diabetes resistant BB or normal Wistar rats. The release of ROI was determined by chemiluminescence using in parallel luminol and lucigenin as detector molecules. In diabetes prone BB rats the spontaneous release of ROI was upregulated in macrophages from different compartments, i.e. peritoneum and spleen. Also, maximal output of ROI after activation of macrophages either in vivo by injection of Corynebacterium parvum or in vitro by LPS and IFN was highest for cells from diabetes prone BB rats. This macrophage abnormality was seen in animals prior to recognizable islet inflammation and also was present at the level of macrophages grown in vitro from precursor cells of diabetes prone BB rats. Hypersecretion of oxygen radicals may contribute to Beta cell loss and diabetes development in BB rats.

引用

页码：93 / 98

页数：6

共 29 条

[1] Eisenbarth G.S., Type I diabetes mellitus. A chronic autoimmune disease, N Engl J Med, 314, pp. 1360-1368, (1986)
[2] Hanenberg H., Kolb-Bachofen V., Kantwerk-Funke G., Kolb H., Macrophage infiltration precedes and is a prerequisite for lymphocytic insulitis in pancreatic islets of prediabetic BB rats, Diabetologia, 32, pp. 126-134, (1989)
[3] Leiter E.H., Prochazka M., Coleman D.L., Animal model of human disease: The non-obese diabetic (NOD) mouse, Am J Pathol, 128, pp. 380-383, (1987)
[4] Kolb-Bachofen V., Epstein S., Kiesel U., Kolb H., Low-dose streptozocin-induced diabetes in mice, Diabetes, 37, pp. 21-27, (1988)
[5] Kolb H., Burkart V., Appels B., Hanenberg H., Kantwerk-Funke G., Kiesel U., Funda J., Schraermeyer U., Kolb-Bachofen V., Essential contribution of macrophages to islet cell destruction in vivo and in vitro, J Autoimmunity, 3, pp. 117-120, (1990)
[6] Nerup J., Mandrup-Poulsen T., Molvig J., Helqvist S., Wogensen L., Egeberg J., Mechanisms of pancreatic β-cell destruction in type I Diabetes, Diabetes Care, 11, pp. 16-23, (1988)
[7] Pukel C., Baquerizo H., Rabinovitch A., Destruction of rat islet cell monolayers by cytokines: Synergistic interactions of interferon-gamma, tumor necrosis factor, lymphotoxin and interleukin I, Diabetes, 37, pp. 133-136, (1988)
[8] Rothe H., Fehsel K., Kolb H., Tumor necrosis factor alpha production is upregulated in diabetes prone BB rats, Diabetologia, 33, pp. 573-575, (1990)
[9] Kroncke K.D., Kolb-Bachofen V., Berschick B., Burkart V., Kolb H., Activated macrophages kill pancreatic syngeneic islet cells via arginine-dependent nitric oxide generation, Biochem Bioshys Res Commun, 175, pp. 752-758, (1991)
[10] Malaisse W.J., Malaisse-Lagae F., Sener A., Pipeleers D.G., Determinants of the selective toxicity of alloxan to the pancreatic B cell, Proc Nat! Acad Sci USA, 79, pp. 927-930, (1982)

← 1 2 3 →