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)

A total of 291 unvaccinated sheep from Brucella melitenesis-infected flocks were examined for delayed-type hypersensitivity (DTH) responses with Brucellergene commercial allergen and with cold saline extract and cytosol from rough B. melitensis 115, and their sera were tested in the rose bengal test (RBT), complement fixation test (CFT), and enzyme-linked immunosorbent assay (ELISA) with lipopolysaccharide. DTH reactions were maximal after 72 h, with no intensity differences among allergens, inoculation sites (eyelid and tail), and doses tested. There were no differences in the results recorded by visual inspection and palpation of inoculation sites, by measuring skin thickness with a caliper, or by microscopic examination of samples taken at necropsy. Six days after DTH testing, energy was observed in 100% of the animals, and 100% reactivity was recovered only after 24 days. All animals were necropsied, and thorough bacteriological searches were performed. The sensitivities found with the 140 animals from which B. melitensis was isolated were ELISA, 100%; DTH, 97.1%; RBT, 92.1%; and CFT, 88.6%. Those results put into question the value of RBT and CFT as screening and confirmatory tests for sheep brucellosis and at least indicate that their standardization should be modified. For 151 tested sheep from which B. melitensis was not isolated, the percentages of positive animals were ELISA, 100%; DTH, 94.0%; RBT, 57.6%; and CFT, 53.6%. All tests were negative for 100 tested sheep from Brucella-free flocks. The different results of bacteriological and immunological tests suggest the usefulness of developing indirect tests able to distinguish truly infected animals from those that have developed an immunological response.
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PMID:Evaluation of allergic and serological tests for diagnosing Brucella melitensis infection in sheep. 798 28

The hypothalamic paraventricular nucleus (PVN) is recognized as a major site of autonomic control, but the role of this nucleus in thermoregulation is unclear. Therefore the role of the PVN in the febrile response and in the maintenance of normal body temperature was investigated. Conscious, unrestrained rats with chronic lesions of the PVN received intracerebroventricular injections of several doses of prostaglandin (PG) E2 or intraperitoneal applications of Escherichia coli lipopolysaccharide. The body temperatures of both lesioned and sham-operated animals, monitored via radio telemetry, were compared. Intracerebroventricular PGE2 at doses of 10, 25, and 50 ng caused dose-dependent fevers in both PVN-lesioned and sham-operated animals, which at lower doses were smaller in the lesioned animals than in the sham-operated animals. Intraperitoneal lipopolysaccharide application, 50 micrograms/kg body wt, evoked a significantly lower febrile response in PVN-lesioned animals than in controls. The body temperature of PVN-lesioned animals and controls showed no difference during 300 min of exposure to heat (32 degrees C) or cold (7 degrees C). These results suggest that the PVN contributes to the complex regulation of temperature during the febrile response but not during the maintenance of normal body temperature.
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PMID:Reduced febrile responses to pyrogens after lesions of the hypothalamic paraventricular nucleus. 804 39

L1 is a cell surface glycoprotein of the immunoglobulin superfamily which was initially shown to mediate adhesion between neural cells. Recently we have reported that L1 is expressed by bone marrow cells and the majority of mature lymphocytes (Kowitz et al., Eur. J. Immunol. 1992. 22: 1199-1205). To analyze the function of L1 on leukocytes we studied its regulation following cell activation. In vitro activation of B lymphocytes with lipopolysaccharide or T lymphocytes with phorbol 12-myristate 13-acetate/Ca2+ ionophore, concanavalin A or anti-CD3 monoclonal antibody as well as in vivo activation of V beta 8+ T cells with staphylococcal enterotoxin B (SEB) revealed a down-regulation of L1 within 48 h. A rapid loss of L1 expression was seen when mouse neutrophils were activated with PMA alone. This rapid loss paralleled the shedding of L-selectin. We also studied a possible role of L1 in the binding of leukocytes to endothelial cells. ESb-MP lymphoma cells with a high expression of L1 (L1hi) could bind to bend3 endothelioma cells without prior activation with inflammatory cytokines. The interaction was inhibited by anti-L1 antibodies. In contrast, ESb-MP cells with low L1 expression (L1lo) were only marginally bound. Latex beads coated with affinity-isolated L1 antigen were also able to bind to the endothelioma cells in a specific fashion. The binding of ESb-MP lymphoma cells required Ca2+ and Mg2+ ions and was sensitive to cold temperature. Since the endothelioma cells did not express L1 the binding mechanism studied here is distinct from the established L1-L1 homotypic interaction. It is possible that the novel L1-mediated adhesion pathway involves an unidentified ligand and could play a role in leukocyte migration.
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PMID:L1 adhesion molecule on mouse leukocytes: regulation and involvement in endothelial cell binding. 822 69

At thermoneutral conditions, high steady-state levels of transcripts for both IL-1 alpha and its receptor IL-1RtI were found in specialized thermogenic organ, brown adipose tissue (BAT) of adult mice, as compared with the levels in lymph nodes, brain and spleen. A pronounced decrease of IL-1 alpha mRNA level in BAT was observed after lipopolysaccharide (LPS) administration and after exposure to cold. Likewise, LPS decreased the IL-1RtI mRNA level and depressed also the expression of cold-inducible genes for the BAT-specific heat-producing uncoupling protein and for lipoprotein lipase. It is concluded that, besides the centrally-mediated effects, there exists a direct peripheral interaction of IL-1 cytokines with BAT cells.
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PMID:Expression of interleukin-1 alpha and interleukin-1 receptor type I genes in murine brown adipose tissue. 822 51

Peripheral vasodilation is a common feature of warm heart surgery and creates clinical concerns when pressor agents become necessary because of the potential for some of these drugs to adversely affect flow through newly engrafted arterial and venous bypass conduits. The possible role of a temperature-dependent production of cytokines in the pathogenesis of this vasodilation was investigated in a two-part study. In part I, lipopolysaccharide-activated peritoneal rabbit macrophages (5 x 10(6)/ml) were incubated at 30 degrees or 37 degrees C up to 9 hours and the concentration of tumor necrosis factor released in the supernatant was serially measured by a bioassay. Tumor necrosis factor production was found to increase over time for each of the two temperatures of incubation but was significantly higher throughout the observation period in normothermic experiments than in those done at 30 degrees C. Part II was a prospective clinical study involving 30 patients who underwent either cold (core temperature 28 degrees to 30 degrees C, n = 15) or warm (37 degrees C, n = 15) cardiopulmonary bypass and in whom serum levels of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 were measured by enzyme-linked immunosorbent assays at 2, 4, 10, and 24 hours after bypass. Cytokine levels were found to be consistently higher in patients having normothermic bypass. Differences between the two groups were significant 2 hours after bypass for tumor necrosis factor alpha and interleukin-6 (p < 0.02 and p = 0.0001, respectively) and 4 and 10 hours after bypass for interleukin-1 beta (p < 0.01 and p < 0.04, respectively). The incidence of vasodilation necessitating vasopressor support was twofold higher in the normothermic group (six patients versus three in the hypothermic group). Taken as a whole, patients supported by pressor agents had significantly higher cytokine levels after bypass than those who did not require pressor therapy. Our results suggest that vasodilation occurring with warm heart operation is, at least partly, mediated by a temperature-dependent release of cytokines. Vasodilation might therefore be mitigated by simply allowing the core temperature to drift during bypass. Our recent clinical experience suggests that this "tepid" heart surgery (32 degrees to 34 degrees C) effectively blunts most of the vasodilatory response to strictly normothermic bypass without compromising maintenance of myocardial aerobiosis during arrest.
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PMID:A potential mechanism of vasodilation after warm heart surgery. The temperature-dependent release of cytokines. 828

The effects of endotoxin (lipopolysaccharide; LPS) on the reactivity of isolated porcine basilar artery were examined using in vitro tissue bath techniques. The active muscle tone of the basilar arterial rings with or without endothelial cells induced by U46619 (1 microM) reached a plateau in 15 min, which was stable for the first hour and gradually decreased during the next 5 h. This time-dependent decrease in tone was significantly potentiated in the presence of LPS (20 micrograms/ml). The potentiation by LPS was blocked by Nw-nitro-L-arginine (L-NNA; 60 microM), methylene blue (10 microM), and dexamethasone (1 microM) but not by hemoglobin (1 microM). The effect of L-NNA was readily reversed by L-arginine but not by D-arginine. Furthermore, the contractile responses of porcine basilar arterial rings with or without intact endothelium to U46619 and KCl were decreased following incubation with LPS (20 micrograms/ml) for 4 h. Similar hyporeactivity was observed in cold storage-denervated cerebral arteries incubated with LPS for 4 h. This decrease in contractile responses in LPS-treated rings was reversed by 60 microM L-NNA and 1 microM dexamethasone. These results indicate that LPS treatment renders the porcine basilar arteries hyporesponsive to vasoconstrictors. Since effects of LPS were not modified by the presence of endothelial cells and perivascular neurons, the alteration in cerebral arterial reactivity may be due in part to an enhanced formation of nitric oxide from L-arginine in the vascular smooth muscle cells.
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PMID:Endotoxin decreases the contractile responses of the porcine basilar artery to vasoactive substances. 831 24

Alterations of cell-mediated immune responses in the rat produced by 5-day (one 3-min stress session each day for 5 days) and 1-day (three 3-min stress sessions within 12 h) cold water stress administration were investigated. Mitogenic responses to concanavalin A (Con A) and lipopolysaccharide (LPS), interleukin-2 (IL-2) production, CD4+/CD8+ T-cell ratios, and natural killer (NK) cell activity of blood and spleen lymphocytes were increased by the 5-day cold water stress. Responses to Con A and LPS, IL-2 production, and CD4+ and CD8+ percentages of blood and spleen lymphocytes were decreased by the 1-day cold water stress. Corticosterone levels were increased by both the 1-day and 5-day cold water stress. Cold water stress, as a natural stressor, may have its own unique pattern of neuroendocrine changes because of the accompanying body temperature variations that may influence immune functions.
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PMID:Modulation of cellular immune responses by cold water swim stress in the rat. 837 69

The studies were conducted on normal, febrile and cold-stressed rabbits. Fever was induced by a single intravenous injection of 1 micrograms/kg of E. coli lipopolysaccharide (LPS). The animals were submerged in ice-water for 20 s and then were kept at -15 degrees C for approx. 8 min., until their body temperature dropped by 3 degrees C. Sodium diethyldithiocarbamate (DTC) was injected i.v. to normal, febrile and cold-stressed rabbits, in a single dose of 2 or 20 mg/kg. The effect of DTC on body temperature, the number of neutrophils in blood, phagocytic activity of neutrophils and their ability to reduce nitroblue tetrazolium (NBT) were evaluated. It was found that DTC administered in a dose of 2 or 20 mg/kg did not affect the body temperature of rabbits. In normal rabbits, DTC did not change the number of neutrophils, but increased their phagocytic activity and ability to reduce NBT. In febrile rabbits, DTC depending on the dose, shortened the stimulating effect of LPS on neutrophil ability to reduce NBT but enhanced and prolonged the effect of pyrogen on neutrophil phagocytic activity. The rabbits treated with DTC prior to hypothermia exhibited shorter neutrophilia resulting from cold stress. In addition, DTC administered to the rabbits before their exposure to cold stress proved to be a partial or even total protection against the decrease in NBT reducing ability and phagocytic activity of blood neutrophils.
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PMID:Modulating effect of sodium diethyldithiocarbamate on neutrophils in normal, febrile and cold-stressed rabbits. 853 9

Immunoregulatory states in acute cold-stressed or cold-acclimatized mice were investigated. When male C57BL/6 mice were exposed to environmental temperature of 5 degrees for 24 hr (acute cold stress), the spleen cells showed depressed proliferative responses to stimulation with concanavalin A (Con A) or lipopolysaccharide (LPS) compared with control mice (reared at 25 degrees). The proportion of Thy-1.2+ cells increased significantly in spleens from these acute cold-stressed mice. The Con A responses of T-enriched cells from acute cold-stressed mice were restored to the normal level by adding plastic-adherent cells from control mice. Further, adherent cells from acute cold-stressed mice markedly suppressed the Con A responses of control spleen cells. Thus, the plastic-adherent cells appeared to be responsible for the suppressed Con A responses. On the other hand, proliferative responses to Con A or LPS were elevated in spleen cells from mice exposed to 5 degrees for 3 weeks (cold acclimatization). A significant decrease of Thy-1.2+ cells was detected in these spleens. It was shown that the enhanced proliferative responses were attributable to functional alterations of the plastic adherent cell population but not to those of lymphoid cell population. These findings indicate that the low or high responsiveness of spleen cells to Con A observed in cold-stressed or cold-acclimatized mice, respectively, may be due to a mechanism including the contrary modulations of functions of cells of mononuclear phagocyte lineage.
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PMID:Immunomodulation by cells of mononuclear phagocyte lineage in acute cold-stressed or cold-acclimatized mice. 855 85

Previous studies from this laboratory had shown that exposure of mice to cold water stress leads to an increase in the secretion of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF alpha) from their peritoneal macrophages. We now report that the secretion of IL-6 from peritoneal macrophages is also increased after cold water stress and that the peptide substance P (SP) participates in this stress-induced response. The stress paradigm involved subjecting male C57BL/6J mice to 5 min swim tests in 10 +/- 2 degrees C water twice daily for 4 d. Cold water stress augments the lipopolysaccharide-induced IL-6 secretion from peritoneal macrophages, elevates immunoreactive SP (iSP) in the peritoneal wash fluid, and reduces iSP in certain peritoneum-containing tissues or organs (i.e., diaphragm, abdominal wall, ileum, and rectum). The 10 d stress time studies indicate that increased IL-6 secretion is positively related to elevated iSP in the peritoneal wash fluid and inversely related to reduced iSP in certain peritoneum-containing tissues. Pretreatment with capsaicin, which depletes SP in the sensory nerve endings, eliminates stress-control differences in the peritoneal wash fluid and in certain peritoneal tissues. Moreover, RP67,580, a specific SP antagonist, eliminates the cold water stress-induced augmentation of IL-6 secretion from peritoneal macrophages. These results suggest that cold water stress promotes the release of SP from peritoneal tissues into the peritoneal cavity, where it participates in the cold water stress-induced macrophage functional alterations.
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PMID:Endogenous substance P mediates cold water stress-induced increase in interleukin-6 secretion from peritoneal macrophages. 864 17


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