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-S (IL-1B) 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.
present study was designed to explicate the role of IL-1 Q on inflammatory revelation of oral tissues in mice biochemically. In the Induced arthritis by injection of 10 ug LPS shown the relaese of 0.93 ug IL-B/joint with a peak
at 4-5 h and diminished at 24h, and the release of TNF a of 1,25pg1ioint with a peak at 2-3h and diminished at 6h. After injection of th IL- R 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 (PGEz) accumulated in the oral tissue with dose dependant.
These elucidated IL-18 to be inflammatory mediator in the early phase of its pathogenesis. Intraoral injection of recombinant IL 1 R induced the proliferation of leukocytes in situ. IL-1 R took an pertinent part in the development of inflammation and the succession of cellular infiltration.
The results exemplify that IL-1 R ulavs a significant role in mediating inflammatory response induced by LPS in oral tissue the inflammatory response is regulated by IL-1 R at an acute phase of pathogenesis
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