Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to determine the effect of an inhibitor of bacterial endotoxin, monophosphoryl lipid A (MLA), on lipopolysaccharide (LPS)-induced prostaglandin E2 (PGE2) formation by human choriodecidua explants incubated in vitro. LPS induced the release of PGE2 from explants in a time-and dose-dependent manner (P < 0.05, n = 5), thus establishing the efficacy of the experimental model. MLA at concentrations of 10 micrograms/ml also increased PGE2 release from explants when compared to vehicle controls (P < 0.05, n = 5). When used at a concentration that did not stimulate PGE2 release (1 microgram/ml), MLA pretreatment, coincubation or a combination of these protocols did not significantly affect LPS-induced PGE2 release. These data establish that MLA does not act by abrogating tissue LPS responsiveness. Under the conditions utilized in this study, MLA acts locally as a low potency 'LPS-like agent'. The previously reported in vivo efficacy of systemically administered MLA may involve the partial depletion or down regulation of LPS response pathways and the subsequent development of LPS tolerance.
Placenta 1997 May
PMID:The effect of monophosphoryl lipid A on lipopolysaccharide-induced prostaglandin E2 release in human choriodecidua. 917 16

Results of our previous study on the immunity of human placenta and amniotic membranes revealed that in majority of cases these organs present constitutive non-specific antiviral immunity in the organ culture (OC) system. It is possible that interferons (IFNs), tumour necrosis factors (TNFs) and interleukin 6 (IL-6) may be responsible for the antiviral effect. Here, the constitutive and lipopolysaccharide (LPS)-induced production of these cytokines and, additionally, interleukin 10 (IL-10) were determined in OC of chorionic villi, decidua and amniotic membranes. Significant amounts of constitutive TNF-alpha (2-64 U/ml), IL-6 (200-12,000 U/ml) and IL-10 (1-70 ng/ml) were detected in the maternal decidua and chorionic villi of placenta. Amniotic membranes produced lower concentrations of the cytokines. LPS increased the production of cytokines from two- to eightfold. In contrast, activity of IFN released spontaneously was found only in four of 50 placentae and amniotic membranes. LPS and Newcastle disease virus (NDV) induced IFN production in the OC system. However, the increase of IFN after induction was also very small (up to 32 U/ml). Individual differentiation in the cytokines production was observed among placentas and amniotic membranes. TNF was identified as type alpha with addition TNF-beta, IFN as type alpha, beta and gamma.
Placenta
PMID:Constitutive and induced cytokine production by human placenta and amniotic membrane at term. 925 Jul 7

The human placental syncytiotrophoblast is derived from differentiating cytotrophoblasts and is in contact with maternal blood. This endothelial function positions the trophoblast to regulate maternal-fetal exchange and to influence circulatory dynamics through paracrine interactions in the placenta. Two isoforms of nitric oxide synthase (NOS) are expressed in placenta, and northern analysis, reverse transcription-polymerase chain reaction (RT-PCR), and immunocytochemistry were used to correlate expression of the type II, inducible NOS (iNOS) and the type III, endothelial NOS (eNOS) with state of differentiation in cultured trophoblast from term placentae. It was also tested whether cytokines known to induce NOS in other cell systems would induce iNOS in human trophoblast. The mRNA for eNOS was detected by RT-PCR, but not by Northern analysis, in cultures grown for 24 h when cytotrophoblasts were dominant. In contrast, eNOS mRNA was abundant in cultures grown for 72 h when syncytiotrophoblast was present. Immunocytochemical staining for eNOS protein showed specific fluorescence in a few cells in cultures at 24 h, but the vast majority of cells expressed eNOS at 72 h. The iNOS isoform was expressed neither basally in any trophoblast culture nor was this isoform induced in cultures exposed to interleukin-1, tumour necrosis factor-alpha, interferon-gamma and lipopolysaccharide. The in vitro pattern of trophoblast eNOS expression models the in vivo pattern of eNOS expression described for villous trophoblast. The results suggest that eNOS plays a role in human trophoblast differentiation and function.
Placenta 1998 May
PMID:Gene expression of nitric oxide synthase in cultured human term placental trophoblast during in vitro differentiation. 963 20

There is strong evidence that prostaglandins E2 and F2alpha (PGE2 and PGF2alpha) are involved in the initiation and maintenance of human parturition and that their production can be stimulated by a number of cytokines and in infection-induced preterm labour by bacterial endotoxin. This study used an intact fetal membrane disk model to investigate the regulation of PGE2 and PGF2alpha metabolism by interleukin-1 beta (IL-1beta) and bacterial endotoxin [lipopolysaccharide (LPS)]. Fetal membrane explants were incubated with IL-1beta (0.1 or 1.0 ng/ml) or LPS (10 ng/ml) for 24 h. A mixture of 3H-prostaglandin (0.1 microCi) and unlabelled prostaglandin (1 microg) was then added at selected times after the addition of inflammatory mediators. The radiolabelled prostaglandins and their metabolites were then extracted from the culture medium and quantified by high-pressure liquid chromatography. Levels of prostaglandin metabolites were generally decreased following incubation with IL-1beta or LPS, which is consistent with a decrease in the activity of 15-hydroxyprostaglandin dehydrogenase (PGDH). It is concluded that IL-1beta and LPS moderately decrease the metabolism of prostaglandins, which may contribute to increasing the local levels of active prostaglandins induced by these stimuli.
Placenta 1998 Nov
PMID:Interleukin-1beta and bacterial endotoxin change the metabolism of prostaglandins E2 and F2alpha in intact term fetal membranes. 985 67

Lactoferrin (LF) has been found in most biological fluids including amniotic fluid and cervical mucus in pregnant women and is released from neutrophils in response to inflammation. It is an important component of the host defence against microbial infections due to its antimicrobial properties. Premature labour is caused by amniotic infection and high concentrations of inflammatory cytokines in amniotic fluid with infection are well established. In the present study, LF levels of intrauterine infection in amniotic fluid were measured and the biological significance of LF was investigated. The effects of LF on IL-6 production in cultured amnion cells were also investigated. The concentrations of LF and IL-6 in amniotic fluid with chorioamnionitis (CAM) were 8.76+/-0.65 microg/ml and 6.92+/-4.88 ng/ml (n = 28), respectively, and both were significantly higher (P<0.01) than those without CAM (0.86+/-0.81 microg/ml and 0.34+/-0.25 ng/ml; n = 31). LF and IL-6 levels were significantly higher (P<0.01) with CAM. A significant positive correlation between LF and IL-6 levels in amniotic fluid was found (r = 0.91, P<0.01). To our knowledge, this was the first study of its kind, which shows that IL-6 production induced by lipopolysaccharide in cultured cells was significantly inhibited below physiological concentration of LF in the amnion. In addition, the immunohistochemical localization of LF in fetal membranes was investigated. In the fetal membranes with CAM, strong positive staining was observed in amniotic and chorionic membranes, with leucocyte migration, while weak staining was observed in membranes without CAM. These results show conclusively that LF suppresses amniotic IL-6 production under the conditions of intrauterine infection.
Placenta
PMID:Amniotic fluid lactoferrin in intrauterine infection. 1019 38

We have previously shown that thioredoxin and thioredoxin reductase were immunohistochemically localized in cytotrophoblasts, decidua and stromal cells in the stem villi of human placenta and that the addition of exogenous thioredoxin and thioredoxin reductase to mitochondrial fractions from human placenta displayed a protective effect on fumarase activity against oxidative stress. In this study, to investigate further the roles of thioredoxin and thioredoxin reductase in protecting pregnancy against oxidative stress, we examined the effect of lipopolysaccharide (LPS), which induces a variety of cytokines and produces radical oxygen species, on the expression of thioredoxin and thioredoxin reductase in mouse placenta. We focused on the placental protective effect in the second trimester, when the onset of placental dysfunction might occasionally lead to a critical state for the fetus. Thus we analysed placentae from mice on day 13 of pregnancy at various time points after they were injected with LPS (50 microg/kg i.p.) or saline as a control. The expressions of thioredoxin and thioredoxin reductase were evaluated by Western blotting and immunohistochemistry. Western blot analysis revealed that LPS approximately quadrupled the expression of both thioredoxin and thioredoxin reductase in the placentae of pregnant mice. When both proteins were localized immunohistochemically, it was found that the decidua and the diploid trophoblasts in the basal zone were intensively stained. Furthermore, the expression of 4-hydroxy-2-nonenal (HNE)-modified proteins, which are markers of oxidative stress, was enhanced in placenta by LPS. Our study suggests that the induced thioredoxin and thioredoxin reductase might protect the placenta from the stress induced by LPS.
Placenta 1999 Sep
PMID:Expression of thioredoxin and thioredoxin reductase in placentae of pregnant mice exposed to lipopolysaccharide. 1045 10

To clarify the biological and pathological features of choriocarcinoma, we evaluated the in vitro production of cytokines by a choriocarcinoma cell line, BeWo. We measured the concentration of interleukin (IL)-6 and IL-8 in the culture media of BeWo cells after stimulation with various modulatory agents of cytokine expression by enzyme-linked immunosorbent assays. Northern blot analysis was used to examine the expression of IL-6 and IL-8 mRNA in these cells. A weak expression of IL-6 and IL-8 was detected in unstimulated BeWo cells by both methods. IL-6 transcription and secretion were dose-dependently enhanced by stimulation with IL-1beta, tumour necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1 and 12-O-tetradecanoyl phorbol-13-acetate (TPA). Forskolin, lipopolysaccharide and interferon-gamma had no effect on these cytokines production. The TNF-alpha-induced secretion of IL-6 was inhibited by dexamethasone. The TPA-induced production of IL-6 was inhibited by 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine and sphyngosine, suggesting the involvement of a protein kinase C-dependent pathway. Levels of IL-8 mRNA and protein were also dose-dependently increased by stimulation with IL-1beta, TNF-alpha and TPA. In contrast to IL-6, the expression of IL-8 was not affected by TGF-beta1. It is suggested that, in addition to the production of steroidal and non-steroidal hormones, these cytokines may serve as part of a cytokine network that modulates the proliferation and angiogenesis of choriocarcinomas.
Placenta 2000 May
PMID:Production of interleukin (IL)-6 and IL-8 by a choriocarcinoma cell line, BeWo. 1083 70

The aim of this study was to elucidate whether a novel mitochondrial antioxidant protein, SP-22, is localized in placenta and whether its expression is induced in placenta of lipopolysaccharide (LPS)-exposed mouse. Western blot analysis of normal human placenta indicated that the SP-22 protein was located in the mitochondrial fraction. Immunohistochemical analysis of SP-22 in normal placenta showed that immunoreactive SP-22 was distributed mostly in cytotrophoblastic cells but with almost no signal in syncytiotrophoblasts. The positive signals were also detected in the decidual cells and stromal cells in stem villi of normal placenta. We also examined LPS-mediated inflammatory placenta on day 13 of pregnancy at various time points after LPS injection (50 microg/kg, intraperitoneally). Western blot analysis indicated that LPS approximately quadrupled the expression of SP-22 in placenta of LPS-exposed mouse. When the SP-22 protein was localized immunohistochemically, the decidua and the diploid trophoblasts in the basal zone were intensively stained in placenta of LPS-exposed mouse compared to the control. The localization and inducible expression of SP-22 protein in placenta suggest a possible role in antioxidant system in mitochondria of normal and inflammatory placentae.
Placenta 2000 Nov
PMID:Expression of mitochondrial thioredoxin-dependent antioxidant protein, SP-22, in normal human and inflammatory mouse placentae. 1109 35

Prenatal exposure to infection appears to increase the risk of schizophrenia and other neurodevelopmental disorders. We have hypothesized that cytokines, generated in response to maternal infection, play a key mechanistic role in this association. E16 timed pregnancy rats were injected i.p. with Escherichia coli lipopolysaccharide (LPS) to model prenatal exposure to infection. Placenta, amniotic fluid and fetal brains were collected 2 and 8h after LPS exposure. There was a significant treatment effect of low-dose (0.5mg/kg) LPS on placenta cytokine levels, with significant increases of interleukin (IL)-1beta (P<0.0001), IL-6 (P<0.0001), and tumor necrosis factor-alpha (TNF-alpha) (P=0.0001) over the 2 and 8h time course. In amniotic fluid, there was a significant effect of treatment on IL-6 levels (P=0.0006). Two hours after maternal administration of high-dose (2.5mg/kg) LPS, there were significant elevations of placenta IL-6 (P<0.0001), TNF-alpha (P<0.0001), a significant increase of TNF-alpha in amniotic fluid (P=0.008), and a small but significant decrease in TNF-alpha (P=0.035) in fetal brain. Maternal exposure to infection alters pro-inflammatory cytokine levels in the fetal environment, which may have a significant impact on the developing brain.
 ...
PMID:Prenatal exposure to maternal infection alters cytokine expression in the placenta, amniotic fluid, and fetal brain. 1116 42

Two serological tests (indirect immunofluorescence and enzyme-linked immunosorbent assay) were developed for the detection of fetal antibody to Chlamydia psittaci. Fetal blood and thoracic fluid from 126 field cases of suspected ovine chlamydial abortion were examined using both tests. Placenta and fetal tissues (lung, liver, and kidney) from the same animals were also examined by the following conventional diagnostic methods: isolation in McCoy cells, detection of chlamydial lipopolysaccharide (LPS), modified Ziehl-Nielsen staining, and direct fluorescent antibody staining of chlamydia in frozen cryostat sections. Seventy cases were positive by fetal serology, and of these, 68 were also positive by isolation and/or LPS detection. The remaining 56 cases had negative fetal serology, and of these, 39 were positive by isolation and/or LPS detection. Results indicate that fetal serology, although less sensitive than either isolation in McCoy cells or detection of chlamydial LPS antigen, may be of particular use when placenta is not available.
 ...
PMID:Detection of chlamydial antibody by fetal serology--an aid to the diagnosis of ovine abortion. 1124 60


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