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Does leptin exhibit cytokine-like properties in tissues of pregnancy?
E B Soh1, M D Mitchell, J A Keelan
1University of Auckland, Faculty of Medicine and Health Sciences, Department of Pharmacology and Clinical Pharmacology, New Zealand. b.soh@auckland.ac.nz
Insights
Gestational leptin does not appear to mediate placental inflammation. However, leptin may influence placental cytokine production, suggesting a regulatory role in pregnancy. Further research is needed for amnion-derived leptin.
Area of Science:
- Reproductive biology
- Endocrinology
- Immunology
Background:
- Leptin, a hormone primarily known for regulating appetite, shares structural similarities with class I cytokines.
- Its presence in gestational tissues raises questions about potential roles in pregnancy, particularly concerning inflammation and immune responses.
Purpose of the Study:
- To investigate whether leptin possesses cytokine-like properties within human gestational tissues.
- To determine leptin's influence on inflammatory modulators and cytokine production in the placenta.
Main Methods:
- Human gestational cells (WISH, JEG3, JAR) and tissue explants (amnion, choriodecidua, placenta) were treated with inflammatory agents (interleukin-1beta, tumor necrosis factor-alpha, lipopolysaccharide) and leptin.
- Leptin production and the release of interleukin-8, interleukin-6, and prostaglandin E2 were measured using immunoassays.
Main Results:
- Leptin production in gestational tissues was not affected by common inflammatory modulators.
- Leptin stimulated the production of interleukin-6 in placental cells and explants.
- Hormones like dexamethasone and insulin influenced leptin production in specific cell lines.
Conclusions:
- Leptin from gestational tissues is unlikely to be involved in placental inflammatory responses.
- Leptin may play a role in regulating cytokine production within the placenta.
- The specific function of leptin derived from the amnion requires further investigation.
Problem:
To determine whether leptin exhibits cytokine-like properties in gestational tissues in light of its homologies with the class I family of cytokines.
Method Of Study:
WISH and JEG3 cells, and amnion and choriodecidua explants, were treated inflammatory modulators (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha] and bacterial lipopolysaccharide [LPS]) and leptin production was measured by immunoassay. Other agents known to regulate adipocyte leptin production were also tested for comparative purposes. In addition, WISH cells, JAR cells and placental explants were treated with leptin to assess its effects on production of IL-8, IL-6 and prostaglandin E2 (PGE2).
Results:
Leptin production by all cells and tissues studied was unaffected by treatment with IL-1beta (2.5 ng/mL), TNF-alpha (25 ng/mL) and LPS (2.5 microg/mL). Dexamethasone stimulated leptin production over two-fold by WISH and JEG3 cells, whereas insulin also stimulated a two-fold increase in leptin production in JEG3 cells. IL-6 production by JAR cells and placental explants was stimulated (two- to three-fold) by leptin (300 ng/mL). PGE2 production was unaffected.
Conclusions:
Leptin derived from gestational tissues is unlikely to play a role in inflammatory reactions within the placenta, but may regulate placental cytokine production. The physiological significance of amnion-derived leptin remains to be established.