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)

Metritis was elicited by intrauterine infusion of tuberculin or killed Campylobacter fetus ssp. venerealis into vaccinated guinea pigs and lipopolysaccharide or immune complexes into normal animals. The local inflammatory response to intrauterine infusion of antigens, lipopolysaccharide, and immune complexes was determined by changes in differential cell counts in the uterine lavage fluid and by histopathological examination of uterine tissue. The percentage of neutrophils was significantly (p less than 0.01) greater in uterine lavage fluid collected at 4 hr after infusion of tuberculin into animals vaccinated locally (intrauterine) with M. tuberculosis than in animals vaccinated parenterally (subcutaneously). In contrast, the local response to infusion with C. fetus ssp. venerealis was approximately the same in animals vaccinated intrauterine and subcutaneously with Campylobacter. The systemic response, measured by the delayed type hypersensitivity cutaneous reaction to intradermal injection of tuberculin, was significantly (p less than 0.01) greater in animals vaccinated subcutaneously than intrauterine. Similarly, the concentration of Campylobacter antibody in the serum of animals vaccinated subcutaneously was significantly (p less than 0.01) greater than in guinea pigs vaccinated intrauterine. The intrauterine infusion of immune complexes, composed of C. fetus ssp. venerealis and corresponding antibody, into the uterus of normal guinea pigs stimulated neutrophil migration into the uterine lumen. Infusion of lipopolysaccharide also stimulated neutrophil migration into the uterine lumen. A correlation between an increased percentage of neutrophils in uterine lavage fluid and infiltration of the uterine epithelium with neutrophils was observed.
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PMID:Immune-mediated migration of neutrophils into the uterine lumen of guinea pigs. 624 31

Immune reactivity of primiparous pregnant C57Bl/6J mice was investigated using in vitro assays of mitogen reactivity. The response to the T cell mitogens phytohemagglutinin (PHA) and concanavalin A of cells from the paraaortic (PA) lymph nodes, which drain the uterus, was decreased in pregnant animals. Reactivity to lipopolysaccharide, a B cell mitogen, was normal. The decreased PHA response was seen with PA cells from mice bearing syngeneic or allogeneic (to DBA/2J) fetuses. It was not due to a change in sensitivity to PHA dose or to active suppression (as demonstrated by mixing experiments). Phytohemagglutinin reactivity of cells from inguinal nodes of pregnant mice showed a more variable depression of response in comparison to that seen with cells from the draining PA nodes. The response of axillary and brachial node cells was similar to virgin values. Statistical analysis revealed no differences in the average number of PA lymphocytes or fetuses per mouse between mice bearing syngeneic or allogeneic fetuses. This parallels the similarities found between syngeneic and allogeneic matings in in vitro functional assays. This study demonstrates that pregnant mice (syngeneic or allogeneic) show only a decrease in T proliferative capacity localized to the area of the uterus, while such responses in the rest of the body are left essentially intact.
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PMID:Cellular immunity during pregnancy. II. Response to T and B cell mitogens. 697 82

The mechanism for the enhancing effect of pyrogen (lipopolysaccharide, LPS) on the fetal toxicity of acetylsalicylic acid (ASA) was studied in pregnant rats. The lethality of ASA was significantly enhanced by LPS in male rats. The fetal toxicity of ASA including fetal death, resorption, growth retardation, and skeletal anomalies (wavy rib and asymmetry of sternebra) was slightly observed in the dams that received a single dose of ASA (125 to 500 mg/kg, p.o.) on the 15th day of gestation, but it was markedly increased by LPS (20 micrograms/kg, i.v.). The enhancement of the toxicity of ASA by LPS was also observed in the maternal body weight gain until term. The plasma concentrations of ASA and salicylic acid (SA), the major metabolite of ASA, were increased by LPS. The tissue concentrations of SA were also increased in the following order: placenta, brain, fetus, uterus, liver and kidney. The ATP levels of placenta and fetus were not influenced by ASA alone, but markedly decreased by both LPS and ASA.
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PMID:[Studies on the pharmacological bases of fetal toxicity of drugs. (I). Relation of fetal toxicity and tissue concentration of acetylsalicylic acid with pyrogen in pregnant rats]. 712 46

Peripheral blood lymphocytes collected from ewes before and during pregnancy manifested constant reactivity to concanavalin A and to paternal and third party peripheral blood lymphocytes. However, in some instances, the reactivity of these maternal cells against lipopolysaccharide and lymphatic lymphocytes from paternal, foetal and third-party donors increased markedly during pregnancy. Apart from an indication that plasma from some pregnant ewes acquired the capacity to depress lymphocyte reactivity non-specifically, no evidence was obtained to suggest that maternal lymphocyte reactivity observed in vitro did not accurately reflect the capacity of these cells in the donor ewe. In particular, there was no indication that populations of maternal peripheral blood lymphocytes returning from the gravid uterus had undergone any modification of reactivity against foetal determinants.
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PMID:Immunological responsiveness of maternal and foetal lymphocytes during normal pregnancy in the ewe. 723 Jan 39

A murine model system was used to study the distribution and regulation of CD14 gene expression in vivo. Western blot analysis failed to detect CD14 in plasma from untreated CB6 (BALB/c x C57Bl6) mice, but showed markedly increased levels of CD14 in plasma from mice treated with lipopolysaccharide (LPS). Plasma levels of CD14 increased in a time- and dose-dependent manner, reaching a maximum between 8 and 16 h. Northern blot analysis of total RNA extracted from mouse tissues revealed low, but significant, levels of CD14 mRNA in many tissues of untreated animals with the highest levels in uterus, adipose tissue, and lung. After intraperitoneal injection of LPS, induction of CD14 gene expression was detected in all organs examined with the extent of induction varying between organs. Induction of CD14 mRNA was both time and dose dependent. Maximum induction in the heart and lung was observed 2-4 h after injection of LPS, while liver and kidney showed maximal induction between 8 and 16 h. In situ hybridization showed that CD14 mRNA was expressed in myeloid cells in many tissues, and that expression in these cells was upregulated by LPS. Unexpectedly, CD14 mRNA was also detected in other cells within tissues, including epithelial cells, and expression in these cell types also was upregulated by LPS. Immunochemical analysis revealed that CD14 antigen colocalized to the cytoplasm of cells expressing CD14 mRNA. These studies demonstrate that CD14 gene expression is not restricted to myeloid cells, and that the level of expression of CD14 is influenced by exposure to LPS.
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PMID:Murine CD14 gene expression in vivo: extramyeloid synthesis and regulation by lipopolysaccharide. 753 83

The regulation of urokinase receptor (u-PAR) gene expression during endotoxemia was studied in vivo with a murine model system. Northern blot analysis demonstrated relatively high levels of u-PAR mRNA in mouse placenta, with intermediate levels in lung and spleen and very low levels in heart and kidney. No u-PAR mRNA could be detected in liver, gut, thymus, brain, or skeletal muscle. Intraperitoneal injection of endotoxin (lipopolysaccharide) increased the steady-state levels of u-PAR mRNA in most tissues examined. The greatest induction (sevenfold) was observed in the lung at 1 hour after injection. The cellular localization of u-PAR mRNA was assessed by in situ hybridization. In control mice, u-PAR mRNA was detected primarily in alveolar macrophages of the lung and lymphocytes of the spleen and thymus, although a specific signal was also present in other cell types. In general, endothelial cells lacked detectable u-PAR mRNA. The induction of u-PAR mRNA by lipopolysaccharide was apparent within 30 minutes and was localized to tissue macrophages, lymphocytes, and endothelial cells lining arteries and veins. At later times (1 to 3 hours), specialized epithelial cells present in gastrointestinal tract, bile ducts, and uterus were also positive for u-PAR mRNA. Induction of u-PAR in vivo by lipopolysaccharide may facilitate the extravasation and migration of leukocytes during inflammation.
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PMID:Endotoxin stimulates expression of the murine urokinase receptor gene in vivo. 767 80

Several mechanisms have been suggested to account for the survival of the semiallogeneic fetus in the maternal uterus. However, no data are available to explain how the blastocyst resists the high number of macrophages in the uterus at the time of implantation. The present study examines the in vitro development of murine 3.5-day-old syngeneic or semiallogeneic blastocysts in the presence of nonactivated or lipopolysaccharide (LPS)-activated macrophages. It was found that the in vitro development of blastocysts was undisturbed by the presence of nonactivated or LPS-activated macrophages. The outgrowing trophoblasts were not only nonadhesive to the macrophages but also repelled them actively, thus preventing them from reaching the inner cell mass (ICM). Removing the zona pellucida by use of pronase or killing the ICM by irradiation did not alter the repulsion of macrophages by the trophoblasts. On the other hand, removal of the trophectoderm by antibody and complement treatment rendered the macrophages adhesive and destructive to the ICM. Four of 15 ICM (27%) were destroyed by nonactivated macrophages, and all of the ICM (15/15) were destroyed by LPS-activated macrophages. It is noteworthy that the addition of colchicine, cytochalasin B, proteinase inhibitors, anti-transforming growth factor-beta (TGF beta) antibodies, and indomethacin had no effect on the repulsion of macrophages by the trophoblasts. Therefore, it seems that microtubular proteins, microfilaments, extracellular matrix-degrading enzymes, TGF beta, and prostaglandins are not involved in the repulsion process. These results indicate that trophoblasts protect the ICM from the destructive action of macrophages by a repulsion mechanism of an as yet unknown nature.
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PMID:Trophoblasts protect the inner cell mass from macrophage destruction. 769 Nov 93

During early human pregnancy, fetal cytotrophoblasts rapidly invade the uterus. This process has many similarities to tumor invasion, except that the extent and the timing of cytotrophoblast invasion are carefully regulated. Therefore, this system is particularly useful for studying mechanisms that regulate invasive processes. Previously, we showed that production and activation of the 92-kDa type IV collagenase (matrix metalloproteinase(MMP)-9) is necessary for cytotrophoblast invasion in vitro. In other systems, interleukin (IL)-1 beta is an important regulator of matrix-degrading metalloproteinases. Therefore, we investigated trophoblast production of IL-1 beta and its receptors, as well as the effects of this cytokine on cytotrophoblast metalloproteinase activity and invasion. The results showed that release of IL-1 beta parallels the invasive potential of the cytotrophoblasts; the highest levels are produced by first trimester cells and the lowest levels by term cells. Immunoprecipitation showed that cytotrophoblasts express the 80-kDa type I IL-1 receptor, suggesting that autocrine effects are possible. IL-1 beta stimulated trophoblast MMP-9 secretion (by a mechanism that required nascent mRNA and protein synthesis) as well as metalloproteinase activity and invasion of Matrigel. Increasing (by lipopolysaccharide treatment) or decreasing (by glucocorticoid treatment) IL-1 beta production had parallel effects on MMP-9 secretion, metalloproteinase activity, and invasion. Because IL-1 beta and corticosteroids are present in high concentrations at the maternal-fetal interface, normal trophoblast invasion may be regulated, in part, by their opposing actions. In contrast, stimulation of cytotrophoblast IL-1 beta secretion by lipopolysaccharide may play a role in the sequela of infected fetal membranes.
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PMID:Interleukin-1 beta regulates human cytotrophoblast metalloproteinase activity and invasion in vitro. 800 17

Human adenoviruses (Ad) contain a complex transcription region (E3) which codes for proteins that interact with several arms of the immune system. However, E3 genes are not essential for replication in tissue culture. An E3-encoded 19,000-molecular-weight (19K) glycoprotein (gp19K) binds to the class I major histocompatibility complex (MHC) in the endoplasmic reticulum and prevents MHC transport to the cell surface. Three other E3 proteins are involved in the inhibition of apoptosis by tumor necrosis factor alpha. The entire E3 genomic DNA was utilized to produce transgenic mice to study the effect of the E3 proteins on pathogenesis of various infectious agents and to investigate the in vivo synthesis and processing of the multiple E3 mRNAs and proteins. There was basal expression of the E3 promoter in the thymus, kidneys, uterus, and testes and at all levels of the gastrointestinal tract. In addition, the E3 promoter of the transgene could be activated in some other organs, including the liver, by infection of these animals with an E3-deficient Ad (Ad7001) which contains a functional E1A region. Transactivation in vivo could also be demonstrated by infusion of bacterial lipopolysaccharide. There appeared to be differential ratios of expression between several of the E3 mRNAs in transgenic lung fibroblasts and primary kidney cells cultured from the transgenic animals. This observation suggested that there was differential mRNA splicing that was organ specific. These transgenic animals should provide a useful model for studying the effects of the E3 proteins on the immune system and on diseases affected either by control of MHC or by selected functions of tumor necrosis factor that are inhibitable by Ad E3 proteins.
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PMID:Characterization of transgenic mice containing adenovirus early region 3 genomic DNA. 805 67

The murine cDNA, encoding the purine catabolic enzyme, ecto-5'-nucleotidase (NT), was cloned and the tissue-specific distribution of both the mRNA and enzyme activity was examined. Starting with kidney RNA and primers based on the known rat sequence, reverse transcriptase-polymerase chain reaction (RT-PCR) was utilized to obtain the complete sequence for the translated portion of the murine cDNA. Murine NT is 94% identical to human NT at the amino acid (aa) level and 86% identical at the nucleotide (nt) level. NT enzyme assays revealed greater than tenfold more NT activity in mature vs. immature murine T- and B-lymphocytes. A similar increase in NT activity was also found when the pre-B-cell line, 70Z/3, was induced to produce surface kappa light chains with lipopolysaccharide (LPS) and gamma-interferon (gamma-IFN). Thus, culture systems in which murine lymphocytes mature may be useful for examining the mechanisms of NT gene regulation, as well as the function of NT in the immune system. In tissues, enzyme activity varied over 30-fold, from the lowest levels in skeletal muscle, thymus and spleen to highest in placenta, kidney and forestomach. Levels of mRNA, as determined by RNase protection assay, showed increased NT expression in the early gestation site, as compared to non-pregnant uterus, and in day-19.5 placenta, as compared to day-13 chorioallantoic placenta. Messenger RNA levels were in general proportional to enzyme activity, except in the lung and glandular stomach where mRNA levels were higher than expected, based on enzyme activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Murine ecto-5'-nucleotidase (CD73): cDNA cloning and tissue distribution. 822 5


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