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

Vitamin D3 at a concentration of 300 nM was shown to significantly reduce the yields of cytotoxin produced by human peripheral blood mononuclear cells. Reduction of cytotoxin titers occurred when induction was performed with either concanavalin A, interleukin 2, or ionomycin. Typing of this cytotoxin was accomplished using antisera that were prepared by immunization of rabbits with either recombinant tumor necrosis factor or lymphotoxin. Both antisera were demonstrated to neutralize the cytotoxic activity produced by the peripheral blood mononuclear cells in the presence or absence of vitamin D3. These latter experiments suggested that the cytotoxin in question might be lymphotoxin. Vitamin D3 was also shown to decrease cytotoxin production by a transformed B-cell line known to produce only lymphotoxin, supporting the concept that this vitamin could diminish yields of lymphotoxin at least under certain circumstances. However, purified adherent cells induced by Escherichia coli lipopolysaccharide produced a cytotoxin that was also inhibited by the presence of vitamin D3. Indomethacin failed to influence the effects of vitamin D3 on the production of the cytotoxin. These studies suggest that vitamin D3 may have a role in regulating the secretion of cytotoxic factors which may be important in the defense against neoplastic diseases.
 ...
PMID:The effect of vitamin D3 on the production of cytotoxic factors by human peripheral blood mononuclear cells. 278 95

Rat Kupffer cells stimulated with bacterial lipopolysaccharide (LPS) produced high levels of interleukin 1 (IL-1), as determined by thymocyte proliferation assay. Indomethacin revealed a dose-dependent augmentation in IL-1 production, in parallel with a dose-dependent reduction in prostaglandin E2 production by Kupffer cells. The addition of exogenous prostaglandin E2, dibutyryl cAMP, or isoproterenol led to a dose-dependent suppression of IL-1 production. The supernatant from LPS-stimulated Kupffer cells also contained factors that inhibited IL-1-induced thymocyte proliferation. Upon gel filtration, two inhibitory peaks, at apparent MW of 27,000 and 6000, were obtained. The latter but not the former fraction also affected interleukin 2 (IL-2)-induced thymocyte proliferation. Increasing amounts of IL-1 overcame the inhibitory activity derived from the 27,000 MW fractions. These results suggest to us that prostaglandin E2 and IL-1 inhibitor released by Kupffer cells may be involved in negative self-control in regulating IL-1 production and its action.
 ...
PMID:Kupffer cells may autoregulate interleukin 1 production by producing interleukin 1 inhibitor and prostaglandin E2. 285 46

In the preceding paper it was shown that Kupffer cells isolated by digestion of the liver and purified by centrifugal elutriation can be activated in vitro by lipopolysaccharide and muramyl dipeptide to an enhanced superoxide response upon zymosan phagocytosis. Lipopolysaccharide and muramyl dipeptide also led to a strongly increased prostaglandin E2 release during the phagocytosis of zymosan. This activation was accompanied by an increased production of prostaglandin E2 during the incubation with the stimuli. Prostaglandin E2 synthesis was inhibited by the cyclooxygenase inhibitor indomethacin, reduced by dexamethasone, but only slightly decreased by the lipoxygenase inhibitor nordihydroguaiaretic acid. Indomethacin and dexamethasone also reduced the superoxide response, which only in the case of indomethacin is reversed by exogenous prostaglandin E2. Dexamethasone reduced the superoxide response in unstimulated cells as well. From these results it is deduced that cyclo-oxygenase products, especially prostaglandin E2, but not lipoxygenase products, i.e. leukotrienes, play some regulatory role in the activation process of Kupffer cells; in addition, a prostaglandin-independent inhibition exerted by dexamethasone seems to exist.
 ...
PMID:Guinea pig Kupffer cells can be activated in vitro to an enhanced superoxide response. II. Involvement of eicosanoids. 285 91

Treatment of BALB/c, C57Bl/6 or C3H/HeJ mice with non-toxic concentrations of indomethacin (75-100 micrograms/day) led to a depression of plasma neutral proteinase activity as determined with an (125I)-caseinolytic assay. Lower concentrations of indomethacin (50 micrograms/day), aspirin (1 mg/day), LiCl (3 meq/kg/day), Sulindac (100 micrograms/day), indomethacin analogs (MK-410, MK-555) or lipopolysaccharide (100 micrograms) did not induce depression in proteinase activity. Indomethacin did not directly inhibit the proteinase activity of normal plasma in vitro. The in vivo effects of indomethacin were reversible and plasma proteinase activity returned to normal values within 8 days of cessation of treatment. These results indicate that indomethacin can uniquely alter plasma proteinase homeostasis in normal mice. While effective in depressing the plasma proteinase activity of normal mice, treatment of mice bearing either the BCL1 leukemia or the B16-F10 melanoma with indomethacin did not depress the elevated plasma proteinase levels detected in tumor-bearing animals. Thus the elevation in proteinases detected in tumor-bearing animals may not be the result of increased prostaglandin synthesis and plasma proteinase activity in such disease states may be regulated differently than in normal mice. However, the ability of this potent anti-inflammatory agent to alter proteinase metabolism may contribute to its therapeutic efficacy in the management of inflammatory disease.
 ...
PMID:Indomethacin induces the suppression of plasma neutral proteinase activity in mice: possible relationship to efficacy as an anti-inflammatory drug and induction of alterations in the immune system. 302 Feb 55

Oncogenic transformation of mouse 10T 1/2 fibroblasts induced upon exposure to X-ray or N-methyl-N'-nitro-N-nitrosoguanidine was suppressed if lipopolysaccharide (LPS) was present in the culture medium. The suppressive effect of LPS was exerted within 24 h after irradiation. Suppression was dependent on the concentration of LPS added and LPS (2 micrograms/ml) derived from Salmonella minnesota R595 reduced the number of transformed type III foci per dish from 0.39 to 0.15. Indomethacin (1 to 30 microM) further enhanced the effect of LPS in a dose-dependent manner.
 ...
PMID:Inhibition of X-ray or chemical carcinogen-induced neoplastic transformation of C3H10T1/2 fibroblasts by lipopolysaccharides. 308 80

The intraperitoneal injection of E. coli extract in the mouse resulted in a biphasic accumulation of leukocytes. The first phase of leukocyte accumulation was based on neutrophil influx in the peritoneal cavity, which occurred 1-2 days after E. coli extract administration. The second phase was based on macrophage influx, which occurred 12 days after E. coli extract administration. Preceding the influx of neutrophils in the first phase, the exudation of plasma proteins in the peritoneal fluid occurred at 4 h. A slight increase in plasma exudation accompanied the macrophage influx in the second phase of leukocyte accumulation. These kinetics of the inflammatory response to E. coli extract were similar to those of the inflammatory response to lipopolysaccharide (LPS), suggesting that the inflammatory response induced by E. coli extract administration was mainly due to the effect of LPS, a component of the E. coli extract. Indomethacin reduced the plasma exudation at 4 h but had no influence on the leukocyte accumulation. On the other hand, dexamethasone suppressed the leukocyte accumulation in both phases.
 ...
PMID:Studies on inflammation in mice: dynamics of inflammatory response induced by extract from Escherichia coli and influence of antiinflammatory drugs. 329 7

We have recently shown that synovial fibroblasts cultured from patients with reactive or rheumatoid arthritis exhibit increased autofluorescence when compared with controls. Morphological studies suggested that this increase was related to the anomalous structure of mitochondria in cells cultured from rheumatoid or non-rheumatoid inflammatory synovial tissue. The present study describes attempts to find an explanation for these observations. The effects of conditioned media of cultured mononuclear cells were tested on normal synovial fibroblasts. Conditioned media of monocytes stimulated with lipopolysaccharide or poly-IC induced an increase in the cellular autofluorescence and changes in the morphology of mitochondria in normal fibroblasts. These changes were indistinguishable from those seen in synovial fibroblasts cultured from various arthritides. Indomethacin or gold salts did not abolish the effects of monocyte-conditioned media. Abnormal mitochondria could not be induced in the presence of cycloheximide. This study describes a new aspect of monocyte-fibroblast interactions during rheumatoid and non-rheumatoid inflammation of synovial tissue.
 ...
PMID:Activated monocytes induce arthritis-associated changes in mitochondria of cultured synovial fibroblasts. 338 30

We have studied the role of prostaglandin E2 on the modulation of tumor necrosis factor by immunologically elicited and lipopolysaccharide treated murine macrophages. Indomethacin, a potent inhibitor of prostaglandin E2 production, caused a dose dependent augmentation of lipopolysaccharide induced tumor necrosis factor production (2-3 fold at 10(-7) molar). Tumor necrosis factor was released into the extracellular environment and no activity was found to be associated with membrane or cytosolic fractions. Prostaglandin E2 added to the lipopolysaccharide treated cultures suppressed tumor necrosis factor in a dose dependent manner. In these studies, 10(-7) molar PGE2 reduced tumor necrosis factor production to basal levels. These data suggest that PGE2 may be a potent autoregulatory factor that dramatically influences tumor necrosis factor production.
 ...
PMID:Regulation of macrophage tumor necrosis factor production by prostaglandin E2. 345 61

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.
 ...
PMID:Fetal stimulation of maternal immunoglobulin production in mice. 386 44

We have investigated the role of arachidonic acid metabolites in the regulation of interleukin-1 production by murine peritoneal macrophages. Indomethacin a potent inhibitor of prostaglandin synthesis caused a dose-dependent augmentation of lipopolysaccharide induced interleukin production (up to 7-fold at 5 microM). In contrast, lipoxygenase inhibitors, nordihydroguarietic acid and nafazatrom had no effect at doses that did not significantly decrease prostaglandin synthesis. Added to lipopolysaccharide stimulated cultures, PGE2 was also augmented by indomethacin but unlike lipopolysaccharide treated cultures was suppressed by nordihydroguarietic acid. These data suggest that arachidonate metabolites may be potent autoregulators of macrophage interleukin-1 production.
 ...
PMID:Arachidonic acid metabolites regulate interleukin-1 production. 392 70


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>