Interleukin-10 inhibition of interleukin-6 in human amniochorionic membrane: transcriptional regulation
Article Abstract:
Interleukin-10 may suppress production of interleukin-6 in human amniotic membrane. Interleukin-6 plays a prominent role in the inflammatory response to uterine infection that triggers premature labor, and while an infection can be treated with antibiotics, the resultant premature labor cannot be stopped. Researchers collected amniotic membranes at cesarean section. When exposed to a culture medium containing a molecule specific to the bacterium Escherichia coli, the membrane produced interleukin-6. However, adding interleukin-10 inhibited interleukin-6 production, and the more interleukin-10 that was added, the less interleukin-6 was produced.
Publication Name: American Journal of Obstetrics and Gynecology
Subject: Health
ISSN: 0002-9378
Year: 1996
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Interleukin-10 and transforming growth factor-beta inhibit amniochorion tumor necrosis factor-alpha production by contrasting mechanisms of action: therapeutic implications in prematurity
Article Abstract:
Transforming growth factor-beta (TGF-beta) and interleukin-10 (IL-10) both appear capable of regulating tumor necrosis factor-alpha (TNF-alpha) production in amniotic membranes but at different points and by different means during the production cycle. TNF-alpha may play a role in the immune response seen in infections associated with premature labor. TNF-alpha production increased in normal amniotic membrane samples stimulated with lipopolysaccharide but decreased when IL-10 was added. TNF-alpha production decreased in the presence of TGF-beta only in the absence of lipopolysaccharide.
Publication Name: American Journal of Obstetrics and Gynecology
Subject: Health
ISSN: 0002-9378
Year: 1997
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Racial disparity in membrane response to infectious stimuli: a possible explanation for observed differences in the incidence of prematurity
Article Abstract:
A study is conducted to compare the immune responsiveness of aminochorionic membranes (AC) derived from African American (AA) and white (C) women to an infectious stimulus ex vivo. The results revealed that although the C group produced more tumor necrosis factor (TNF), they also produce higher sTNFRs, that may serve as a protective role and that the increased matrix metalloproteinase 9 (MMP9) release by the AA group may indicate greater risk of premature rupture of membranes in the AA group.
Publication Name: American Journal of Obstetrics and Gynecology
Subject: Health
ISSN: 0002-9378
Year: 2004
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