ISSN:
1432-0428
Schlagwort(e):
Key words Autoimmunity
;
diabetes mellitus
;
interleukin-1
;
nitric oxide
;
nitric oxide synthase
;
NOD mice
;
pancreatic islets
;
polymerase chain reaction.
Quelle:
Springer Online Journal Archives 1860-2000
Thema:
Medizin
Notizen:
Summary Interleukin-1 β (IL-1 β) has been suggested to mediate beta-cell destruction in insulin-dependent diabetes mellitus (IDDM) by inducing nitric oxide production. In this study, we assessed the levels of IL-1 β and the inducible form of nitric oxide synthase (iNOS), using a semi-quantitative polymerase chain reaction assay, and performed determinations of nitrite accumulation and IL-1 β bioactivity, on pancreatic islets isolated from 5- and 16-week-old female and male nonobese diabetic (NOD) mice and from non-diabetes prone NMRI mice. NOD mouse islets contained notable amounts of IL-1 β mRNA. At 5 weeks of age, but not at 16 weeks, the values were higher in islets isolated from NOD females compared to males. The IL-1 β bioactivity showed differences roughly reflecting the mRNA levels in the NOD mouse islets. In the NMRI mouse islets the IL-1 β bioactivity was very low. The expression of iNOS mRNA increased in both male and female islets between 5 and 16 weeks of age. Immunocytochemistry of pancreatic sections indicated the presence of macrophages especially in the peri-insular area of the NOD mice which suggests that IL-1 β was produced by macrophages. The levels of IL-1 β activity and mRNA in freshly isolated islets from NOD 5-week-old females did not correlate to the iNOS mRNA content or to the nitrite production. However, after incubation with IL-1 β in vitro, both NOD and NMRI islets responded with a marked increase in nitric oxide production. It is concluded that the presence of IL-1 β in isolated NOD mouse islets, via an induction of iNOS expression and nitric oxide production, cannot explain the gender difference in diabetes incidence in NOD mice. [Diabetologia (1995) 38: 153–160]
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1007/BF00400089
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