Interleukin-4 differentially regulates prostaglandin production in amnion-derived WISH cells stimulated with pro-inflammatory cytokines and epidermal growth factor
| Autor: | Timothy A. Sato, J.S. Gilmour, Nuala A. Helsby, Murray D. Mitchell, Jeffrey A. Keelan, W.R. Hansen, D.K. Gupta |
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| Rok vydání: | 1999 |
| Předmět: |
medicine.medical_specialty
Time Factors Clinical Biochemistry Prostaglandin Dinoprostone Phospholipases A Cell Line Proinflammatory cytokine chemistry.chemical_compound Phospholipase A2 Fetal membrane Epidermal growth factor Internal medicine medicine Animals Amnion Arachidonic Acid Epidermal Growth Factor biology Tumor Necrosis Factor-alpha Interleukin Cell Biology Rats Isoenzymes Phospholipases A2 medicine.anatomical_structure Endocrinology chemistry Eicosanoid Cyclooxygenase 2 Prostaglandin-Endoperoxide Synthases Prostaglandins biology.protein Cytokines Interleukin-4 Interleukin-1 |
| Zdroj: | ResearcherID |
| ISSN: | 0952-3278 |
| DOI: | 10.1054/plef.1999.0033 |
| Popis: | Cytokines and growth factors have been proposed to act as in vivo modulators of amnion prostaglandin production at parturition. To characterize the effects of the 'anti-inflammatory' cytokine interleukin (IL)-4 on amnion prostaglandin production, amnion epithelium-derived WISH cells were treated with IL-4 in the presence/absence of IL-1beta, tumour necrosis factor-alpha (TNF-alpha) or epidermal growth factor (EGF). IL-4 (0.08-10 ng/ml) potently inhibited cytokine-stimulated PGE2 production over 16 h (maximal inhibition approximately 66% at 2.0 ng/ml IL-4). Delaying addition of IL-4 (1 ng/ml) by up to 8 h after IL-1beta addition only slightly attenuated its inhibitory effects, from approximately 65% to approximately 50%. EGF-stimulated PGE2 production was either not inhibited or slightly stimulated by IL-4. Immunoblotting studies revealed that IL-4 (10 ng/ml) significantly suppressed prostaglandin-H synthase-2 (PGHS-2) levels in cells stimulated with IL-1beta and TNF-alpha over 16 h, but had no consistent effects on cytosolic phospholipase A2 (cPLA2) levels under any condition. In the presence of arachidonic acid (10 microM), IL-4 again inhibited cytokine-stimulated, but not EGF-stimulated, PGE2 production. The presence of IL-4 also failed to alter the amount of arachidonic acid released in response to EGF. These findings suggest a role and potential therapeutic application for IL-4 in inhibiting amnion PGHS-2 expression and hence prostaglandin production in infection-driven preterm labour, but not labour in the absence of inflammatory initiators. |
| Databáze: | OpenAIRE |
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