A biochemical investigation of the IL-1beta role of upon inflammation in mouse.
- Author:
Duk Sang LEE
1
;
Ki Soo LEE
Author Information
1. Department of Orthodontics, Graduate School, Kyung Hee University, Korea.
- Publication Type:Original Article
- Keywords:
IL-beta;
inflammation;
lose of proteoglycan;
cyclooxygenase metabolites
- MeSH:
Animals;
Arthritis;
Cytokines;
Homeostasis;
Inflammation*;
Interleukins;
Joints;
Leukocytes;
Mice*;
Necrosis;
Negotiating;
Proteoglycans
- From:Korean Journal of Orthodontics
1998;28(4):611-626
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Cytokines are intercellular peptide mediators that regulate homeostasis and host defense reactions in living body. Of the diversity of cytokines in terms of biological accomplishment, interleukin 1-beta (IL-1beta) and tumor necrosis factor(TNF) are the most conspicuous cytokines with a wide variety of effects on cells involved in inflammatory and immune responses, and likely to be involved in the inflammatory pathogenesis of oral tissue as well. The present study was designed to explicate the role of IL-1beta on inflammatory revelation of oral tissues in mice biochemically. In the Induced arthritis by injection of 10 microgram LPS shown the relaese of 0.93 microgram IL-beta/joint with a peak at 4-5 h and diminished at 24h, and the release of TNF alpha of 1.25microgram/joint with a peak at 2-3h and diminished at 6h. After injection of th IL-beta into the joint, the member of leucocytes proliferated with a peak at 4-5h and diminished at 36h and the loss of proteoglycan showed with maximum at 15-30h. After injection of IL-1,6 into the oral tissue, cycloosygenase metabolites (PGE(2)) accumulated in the oral tissue with dose dependant. These elucidated IL-1beta to be inflammatory mediator in the early phase of its pathogenesis. Intraoral injection of recombinant IL 1beta induced the proliferation of leukocytes in situ. IL-1beta took an pertinent part in the development of inflammation and the succession of cellular infiltration. The results exemplify that IL-1beta ulavs a significant role in mediating inflammatory response induced by LPS in oral tissue the inflammatory response is regulated by IL-1beta at an acute phase of pathogenesis.
