PubMed · 14479482
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
D A NICKERSON. 1961-11-18. Amniotic fluid embolism.. https://doi.org/10.1001/jama.1961.73040460028017
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Perinatal infections are a risk factor for fetal neurological pathologies, including cerebral palsy and schizophrenia. Cytokines that are produced as part of the inflammatory response are proposed to partially mediate the neurological injury. This study investigated the effects of intraperitoneal injections of lipopolysaccharide (LPS) to pregnant rats on the production of cytokines and stress markers in the fetal environment. Gestation day 18 pregnant rats were treated with LPS (100 microg/kg body wt i.p.), and maternal serum, amniotic fluid, placenta, chorioamnion, and fetal brain were harvested at 1, 6, 12, and 24 h posttreatment to assay for LPS-induced changes in cytokine protein (ELISA) and mRNA (real-time RT-PCR) levels. We observed induction of proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) as well as the anti-inflammatory cytokine IL-10 in the maternal serum within 6 h of LPS exposure. Similarly, proinflammatory cytokines were induced in the amniotic fluid in response to LPS; however, no significant induction of IL-10 was observed in the amniotic fluid. LPS-induced mRNA changes included upregulation of the stress-related peptide corticotropin-releasing factor in the fetal whole brain, TNF-alpha, IL-6, and IL-10 in the chorioamnion, and TNF-alpha, IL-1 beta, and IL-6 in the placenta. These findings suggest that maternal infections may lead to an unbalanced inflammatory reaction in the fetal environment that activates the fetal stress axis.
One of the mysteries of pregnancy is why a mother does not reject her fetuses. Cytokine-modulation of maternal-fetal interactions is likely to be important. However, mice deficient in transforming growth factor-beta1 (TGF beta 1) and other cytokines are able to breed, bringing this hypothesis into question. The phenotype of TGF beta 1 null-mutant mice varies with genetic background. We report here that, in outbred mice, the loss of TGF beta 1-deficient embryos is influenced by the parity of their mother. This is consistent with the loss of mutants being due to immune rejection. An inbred line of TGF beta 1(+/-) mice that supported TGF beta 1-deficient fetuses had high levels of TGF beta 1 in their plasma. Analysis of the amniotic fluids in this line indicated that biologically relevant levels of maternal TGF beta 1 were present in the TGF beta 1(-/-) fetuses. These data are consistent with maternal and fetal TGF beta 1 interacting to maintain pregnancy, within immune-competent mothers.
Surfactant protein D (SP-D) plays a role in innate immunity against various pathogens and in vivo studies have demonstrated that SP-D also has anti-inflammatory properties. SP-D was originally demonstrated in alveolar type II cells, but recent studies have shown extrapulmonary expression of SP-D indicating a systemic role for the protein. This study describes the presence of SP-D in the female genital tract, the placenta and in amniotic fluid using immunohistochemistry and enzyme-linked immunosorbent assay. SP-D was observed in cells lining surface epithelium and secretory glands in the vagina, cervix, uterus, fallopian tubes and ovaries. In the placenta, SP-D was seen in all villous and extravillous trophoblast subpopulations. Endometrial presence of SP-D in non-pregnant women varied according to stage of the menstrual cycle and was up-regulated towards the secretory phase. It is suggested that endometrial SP-D may prevent intrauterine infection at the time of implantation and during pregnancy.