Abstract：
: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 E2 (PGE2) 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-1beta (IL-1beta) and the expression of mRNA for IL-1beta, indicating that this cytokine has a broad anti-inflammatory effect. Transforming growth factor-beta1 (TGF-beta1), which is generally considered to be anti-inflammatory had opposite effects on PGE2 production, in that it increased the output of PGE2 for up to 8 hr. TGF-beta1 increased levels of type-2 cyclo-oxygenase (COX-2) and cytosolic phospholipase A2 (cPLA2) protein, and also activated the cPLA2 enzyme present; the profile of effects is similar to that of the pro-inflammatory cytokine IL-1beta, and was not expected. Combinations of TGF-beta1 with IL-1beta also increased PGE2 output and caused appropriate changes in prostaglandin pathway enzymes, whereas TGF-beta1 and IL-1alpha had more limited effects. Further studies are needed to establish the physiological significance of these findings, but TGF-beta1 does not seem to act as an inhibitory cytokine in intact fetal membranes at term.
journal_name
Immunologyjournal_title
Immunologyauthors
Brown NL,Alvi SA,Elder MG,Bennett PR,Sullivan MHdoi
10.1046/j.1365-2567.2000.00942.xkeywords:
subject
Has Abstractpub_date
2000-01-01 00:00:00pages
124-33issue
1eissn
0019-2805issn
1365-2567pii
imm942journal_volume
99pub_type
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