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)

Granulocyte-macrophage colony stimulating factor (GM-CSF) is one of a number of lympho-haemapoietic cytokines, including CSF-1, interleukin-6 (IL-6) and leukaemia inhibitory factor (LIF) now known to be synthesized by epithelial cells in the murine uterus. GM-CSF synthesis is regulated primarily by the ovarian steroid hormone oestrogen, but is also subject to modulation by factors including a seminal component of seminal vesicle origin which stimulates a 20-fold increase in luminal fluid content at mating, and bacterial lipopolysaccharide (LPS) and the T-lymphocyte and natural killer (NK) cell product interferon-gamma (IFN gamma). In the non-pregnant mouse GM-CSF synthesis peaks at oestrus. Synthesis is maintained at comparable or moderately higher levels during the preimplantation period of pregnancy and in the non-decidualized endometrium during mid gestation. An embryotrophic activity is suggested by studies in vitro that indicate that GM-CSF stimulates attachment and outgrowth of blastocysts. It is postulated that GM-CSF is of major importance to the physiology of pregnancy through its role as a component of a local cytokine circuit acting to recruit and regulate function of endometrial leukocytes, and by its action as interlocutor and important effector arm in embryo-maternal interactions during gestation.
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PMID:Granulocyte-macrophage colony stimulating factor (GM-CSF): one of a family of epithelial cell-derived cytokines in the preimplantation uterus. 146 94

During the second half of murine pregnancy there is a characteristic increase in the number of spontaneous immunoglobulin-secreting cells in the maternal spleen (IgM, IgG and IgA), the uterus-draining lymph nodes (IgG) and Peyer's patches (IgA). There are indications that signals originating from the feto-placental unit are of importance for the generation of at least some of these changes. To evaluate further the role of placental factors as regulators of maternal Ig-secretion, placental extract (PE) was separated into eight fractions by gel-chromatography and each fraction was screened for its effect on splenic (1) background DNA-synthesis, (2) background Ig-secretion and (3) Ig-secretion in lipopolysaccharide (LPS) activated B-cells (anti-Thy1.2 + complement-treated splenocytes). Similarly prepared extracts of fetuses, maternal spleen and maternal liver served as controls. All tissue extracts and splenocytes were syngeneic to avoid reaction to allogeneic determinants. Placental extract fractions did not differ significantly from the other tissue extracts in affecting background lymphocyte activity. However, fraction number 3 from placental extract (PE3, corresponding to an approximate molecular weight of 18-70 kDa) was found strongly to increase the number of IgA-secreting cells (P less than or equal to 0.001) in LPS-activated B-cells. This effect was absent or much less pronounced in the corresponding controls. Blocking of PE3-activity by antibodies against rat prolactin indicated that the enhancing activity may be attributed to proteins of the prolactin/placental lactogen/growth hormone family. This assumption was further strengthened by experiments demonstrating that prolactin exerted preferential enhancement of IgA secretion when added to LPS-activated B-cell cultures in vitro. The possible role of placental prolactin-like molecules as regulators of maternal IgA secretion is discussed.
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PMID:A fraction of murine placental extract enhances IgA production in cultured splenocytes. 154 31

Abnormal parturition can be followed by a persistent endometritis which can have deleterious effects on the cow's subsequent reproductive performance. Normal and active uterine defense mechanisms have been reported to be very important for the exclusion of bacterial infection from the uterus and recovery from endometritis developing after parturition. Despite the widespread use of local or systemic antibiotics, antiseptics, sulfonamides and hormones, rates of recovery from endometritis and the cow's subsequent fertility have not increased appreciably. Furthermore, the cost of any treatment, the frequency of its administration and the milk disposal after treatment make their use uneconomic. Alternative therapies which stimulate the natural uterine defense mechanisms have been suggested as treatments of bovine endometritis. These include: (I) Endotoxins such as lipopolysaccharide of E. coli, (II) serum, plasma or hyperimmune serum, (III) polymorphonuclear leucocyte (PMN) extracts and components and (IV) granulocyte-macrophage colony stimulating factors (G-M CSF).
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PMID:Bovine endometritis: current and future alternative therapy. 177 86

The secretory immune system in the female reproductive tract is known to be regulated by sex hormones and antigen. The purpose of the present study was to examine the control by interferon-gamma (IFN gamma) of the secretory component (SC), the polymeric immunoglobulin A (IgA) receptor, and IgA in uterine secretions and to determine whether IFN gamma influences the proliferation of spleen cells in response to mitogens. When measured by RIA, SC levels in uterine secretions were elevated when increasing doses of IFN gamma (1000-5000 U/uterus) were placed in the uterine lumen of ovariectomized rats. In contrast, IFN alpha-beta (5000 U/uterus) placed in the uterine lumen had no effect on uterine SC levels. To determine whether IgA movement increases in response to IFN gamma, animals were treated with estradiol to increase uterine tissue IgA levels without stimulating the accumulation of IgA or SC in uterine secretions. Under these conditions, intrauterine IFN gamma increased SC and IgA levels in uterine secretions, suggesting that in vivo IFN gamma stimulation of uterine SC increases the transport of IgA from tissue to lumen. Analysis of uterine tissues indicated that intrauterine IFN gamma had no apparent effect on epithelial cell morphology. In contrast, intraepithelial lymphocytes and polymorphonuclear leucocytes, which were sparse in control tissues, increased markedly with IFN gamma treatment. This increase was antagonized when estradiol was administered along with IFN gamma. In other studies, IFN gamma placed in the uterine lumen significantly increased spleen cell proliferation in response to Concanavalin-A, phytohaemagglutinin, and lipopolysaccharide mitogens relative to those in spleen cells from control animals. These studies demonstrate that in vivo treatment with IFN gamma stimulates the mucosal immune system in the female reproductive tract by increasing SC and IgA levels in the uterine lumen and promoting the infiltration of intraepithelial lymphocytes and polymorphonuclear leucocytes into uterine tissue. Further, it suggests that antigen, in stimulating a local uterine response, may act through cytokines, particularly IFN gamma, to regulate the transport of IgA into uterine secretions as well as modulate lymphocyte proliferation at sites distal to the uterus.
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PMID:Cytokine regulation of the mucosal immune system: in vivo stimulation by interferon-gamma of secretory component and immunoglobulin A in uterine secretions and proliferation of lymphocytes from spleen. 195 78

The course of the inflammatory reaction in the uterus after local or systemic administration of specific or non-specific antigens was studied. The study was carried out on 40 cows, 10-11 weeks after labour and between 6 and 8 days after ovulation. A specific cell-mediated type of reaction was induced by intrauterine challenge with PPD in cows previously vaccinated with M. bovis subcutaneously or by intrauterine administration. A specific inflammatory process of the type of Arthus reaction was induced by intrauterine challenge with C. fetus ssp. veneralis in animals immunized with these bacteria subcutaneously or by intrauterine instillation of these bacteria. A non-specific inflammatory process in the uterus was initiated by one instillation of lipopolysaccharide (LPS) into the left uterine horn. The cells were washed out from the uterus before and 6, 24, 48 and 72 hours after initiation of the specific or non-specific inflammatory process. The per cent proportions of various cell types were determined. It was demonstrated that intrauterine instillation of specific or non-specific antigens in cows caused a significant rise in PMNs per cent in relation to the control group.
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PMID:Immunological induction of endometritis-model investigations in cows. 211 51

Bacterial endotoxin-lipopolysaccharide (LPS) rapidly induced hepatic metallothionein (MT) mRNA levels in the LPS-sensitive CD-1 strain of mice. This LPS effect was severely attenuated in the LPS-resistant C3H/HeJ strain of mice, but could be mimicked by injection of human recombinant interleukin-1 alpha (IL-1 alpha) or human recombinant tumor necrosis factor (TNF-alpha). In the CD-1 strain, LPS induction of MT gene expression occurred in each of 10 organs examined (liver, kidney, pancreas, intestine, lung, heart, brain, ovary, uterus, and spleen). Solution hybridization with probes specific for MT-I or MT-II mRNA established that these genes were co-induced in each of the organs and that the liver and kidney contained the highest absolute levels of these mRNAs, whereas in the intestine and spleen they were 10-20-fold lower. LPS and cytokine induction of hepatic MT gene expression occurred in hypophysectomized mice, which suggests a lack of significant involvement of glucocorticoids. Several recombinant cytokines (TNF-alpha, IL-1 alpha, IL-1 beta, IL-6, interferon-gamma (IFN-gamma), as well as poly(rI.rC) were effective inducers of hepatic MT-I and MT-II genes. As an attempt to determine which of these cytokines may mediate LPS effects on MT gene expression in vivo, CD-1 mice were injected with LPS or various cytokines, and RNA from liver, ovary, and uterus was extracted at various times postinjection and analyzed by Northern blotting using probes specific for IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, and MT mRNA. In each organ examined, LPS, IL-1 alpha, or IL-1 beta injection caused a rapid, coordinate, transient increase in the levels of each of the cytokine mRNAs which peaked by 1 h and declined to low levels by 4 h. In contrast, levels of MT mRNA did not reach a peak until 4-6 h postinjection. TNF-alpha had minimal effects on expression of cytokine and MT genes in organs other than liver. IL-6 had no effect on hepatic cytokine mRNA levels, and induced MT mRNA only in the liver which suggests a direct effect of IL-6 on hepatic MT gene expression. These data suggest that the acute effects of LPS on MT gene expression may include complex paracrine interactions between a variety of cytokines and the cells expressing MT genes in each organ, and tissue-specific cytokine effects on the MT genes.
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PMID:Endotoxin induction of murine metallothionein gene expression. 220 73

Bovine uterine defense mechanisms during physiological and pathological conditions have been reviewed in this article. The initial uterine defense against bacterial infection is phagocytosis by uterine leucocytes (mainly neutrophils). The reported literature showed that very little work has been done on immunoglobulins and their role in the bovine uterine defense mechanisms; however, some investigators have found a positive correlation between gamma-globulin and the development of uterine infection after calving. Many explanations exist for the difference in susceptibility of the uterus to infection during the different phases of estrous cycle; however, most of the reports agreed that the uterine defense mechanism is inadequate during diestrus. The abnormal puerperium effects uterine defense mechanisms adversely and prolongs the time to complete uterine involution. Future treatment may utilise natural antimicrobial substances such as proteins or peptides derived from PMN, chemoattractant substances such as E. coli lipopolysaccharide or a bacteria-free filtrate of streptococci. Specific hyperimmunserum could also be used as opsonin for refractory cases of uterine bacterial infections.
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PMID:Bovine uterine defense mechanisms: a review. 269 49

The uterine responses after the infusion of saline (PBS), a bacterial suspension, or lipopolysaccharide derived from Escherichia coli, and after stimulation of the reproductive tract were compared. All infusions provoked a response involving both serum proteins and leucocytes. Protein levels peaked within a few hours of infusion, whereas leucocyte concentration peaked later at around 6 h. Bacterial recovery from the uterus followed a similar pattern, with recovery falling dramatically by 12 h. In mares known to be susceptible to infection large numbers of bacteria were again recovered after 24 h. No differences were apparent between resistant and susceptible mares in protein or leucocyte concentrations. Stimulation of the cervix and uterus resulted in a protein and neutrophil response. In contrast, vaginal stimulation failed to provoke the uterine defences.
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PMID:Dynamics of the acute uterine response to infection, endotoxin infusion and physical manipulation of the reproductive tract in the mare. 331 41

Potassium thiocyanate extracts of a virulent Pasteurella multocida 3:A rabbit isolate were prepared and used as a vaccine in rabbits. The extract contained protein, carbohydrate, hyaluronic acid, lipopolysaccharide, DNA, and RNA. The protein and lipopolysaccharide profiles of the extract were similar to those of the P. multocida cell membrane. Rabbits were vaccinated intranasally (i.n.) or intramuscularly (i.m.) four times at 1- or 3-week intervals and challenged i.n. with the homologous P. multocida 2 weeks after the last vaccination. Rabbits vaccinated with the extract by the i.n. route developed persisting serum immunoglobulin G (IgG) and nasal IgA antibodies, whereas rabbits immunized by the i.m. route produced persisting serum IgG and transient nasal IgA antibodies. The extract prevents the death of rabbits which were vaccinated by either route and challenged. Vaccination by the i.n. route in rabbits reduced the numbers of virulent P. multocida in nasal cavities and lungs and the prevalence and severity of rhinitis and pneumonia. These i.n.-vaccinated rabbits were also resistant to virulent P. multocida colonization in liver, spleen, uterus, and tympanic bullae. Similarly, i.m. vaccination in rabbits resulted in a reduction in the severity of rhinitis; the numbers of virulent P. multocida in lungs; and the prevalence of colonization in liver, spleen, uterus, and tympanic bullae. Vaccination by the i.n. route was superior to that by the i.m. route in that there was a significant reduction in the severity of pneumonia and numbers of virulent P. multocida in nasal cavities and lungs. Rabbits vaccinated with the extract without challenge showed no lesions.
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PMID:A potassium thiocyanate extract vaccine prepared from Pasteurella multocida 3:A protects rabbits against homologous challenge. 367 40

Within 12-24 h of parturition in mice, there was a dramatic increase in the number of immunoglobulin secreting cells in the paraaortic lymph nodes (PALN) draining the pregnant uterus. Compared with stimulation with lipopolysaccharide the ratio of IgG:IgM forming cells was very high in PALN draining a pregnant uterus. The response was eliminated when fetectomy (ablating the embryo but leaving the placenta intact) was carried out on the 12th day of pregnancy. With unilateral fetectomy the uterine horn with intact fetal/placental units can be used as a positive control since lymphoid drainage is laterally confined. Neither healthy (gross and histological criteria) nor partly necrotic placentae stimulated Ig secreting cells in the PALN. The placentae of bilaterally fetectomized females were delivered apparently normally and at about the same time as normal (control) fetuses. Injection of prostaglandin E-2 or F-2 alpha into the tail base led to the appearance of Ig-forming cells in the PALN of normal (virgin) female mice. Indomethacin fed to the pregnant female greatly reduced the numbers of these cells in the PALN. We conclude that the observed local stimulation of maternal Ig production by the fetus may be involved in the transplacental transfer of Ig from mother to fetus.
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PMID:Fetal stimulation of maternal immunoglobulin production in mice. 386 44


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