| Autor: |
Brown, N. L., Alvi, S. A., Elder, M. G., Bennett, P. R., Sullivan, M. H. F. |
| Předmět: |
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| Zdroj: |
Immunology; Jan2000, Vol. 99 Issue 1, p124, 10p |
| Abstrakt: |
Prostaglandins are some of the main mediators which control parturition, and their production by intrauterine tissues can be up-regulated by pro-inflammatory cytokines. Anti-inflammatory cytokines may oppose these effects, and in this study we have investigated how two such cytokines affected fetal membrane function. Interleukin-10 (IL-10) inhibited the output of prostaglandin E[sub 2] (PGE[sub 2]) from intact fetal membranes under basal and lipopolysaccharide (LPS)-stimulated conditions, and there was a parallel decrease in the expression of mRNA for COX-2. IL-10 also inhibited the production of interleukin-1β (IL-1β) and the expression of mRNA for IL-1β, indicating that this cytokine has a broad anti-inflammatory effect. Transforming growth factor-β1 (TGF-β1), which is generally considered to be anti-inflammatory had opposite effects on PGE[sub 2] production, in that it increased the output of PGE[sub 2] for up to 8 hr. TGP-β1 increased levels of type-2 cyclo-oxygenase (COX-2) and cytosolic phospholipase A[sub 2] (cPLA2) protein, and also activated the cPLA[sub 2] enzyme present; the profile of effects is similar to that of the pro-inflammatory cytokine IL-1β, and was not expected. Combinations of TGF-β1 with IL-1β also increased PGE[sub 2] output and caused appropriate changes in prostaglandin pathway enzymes, whereas TGF-β1 and IL-1α had more limited effects. Further studies are needed to establish the physiological significance of these findings, but TGF-β1 does not seem to act as an inhibitory cytokine in intact fetal membranes at term. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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