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)

Studies in our laboratory with both the monkey and the rat showed that, after three hours of endotoxemia, there was a significant decrease in the number of circulating platelets, total hemolytic complement (CH 50 units), and blood serotonin (5-HT) levels. Administration of dexamethasone sodium phosphate in the clinical dose range at the time of endotoxin challenge significantly attenuated the decrease in blood 5-HT levels when compared to the untreated groups in both the monkey and the rat experiments. In the monkey, CH 50 units remained at a higher level when dexamethasone was administered; however, the difference between the treated and untreated groups was not statistically significant. The number of circulating white blood cells and platelets did not appear to be significantly altered by corticosteroid treatment. It is suggested that glucocorticoids may interfere with lipopolysaccharide-induced alterations in complement components or factors regulating hemostasis that influence platelet 5-HT release.
 ...
PMID:Endotoxin-challenged monkeys and rats. 41 99

Staphylococcal enterotoxin B (SEB) was tested in rodent mast cell cultures for the release of serotonin. Both rat RBL-2H3 mast cells and murine peritoneal cells released serotonin after SEB stimulation in culture. Release of serotonin in RBL-2H3 cells depended on the concentration of SEB; an appreciable release was seen at 50 micrograms/ml. The release of serotonin was not due to cell death. Serotonin release could be enhanced by bradykinin but not by vasoactive intestinal peptide, substance P, lipopolysaccharide from Salmonella typhimurium, the calcium ionophore A23187, acetylcholine, adenosine, 5-hydroxyeicosatetraenoic acid, indomethacin, or phorbol myristate acetate. SEB bound directly to the membrane of RBL-2H3 mast cells, and the SEB-binding site, the presumptive receptor, appeared to be a protein. The SEB receptor could not be capped under membrane-capping conditions, and serotonin release could not be enhanced by attempts to cross-link the receptor. These results suggest that mast cells may be an important cell type involved in SEB toxicosis and that release of serotonin may be enhanced by activation of the kinin-kallikrein system.
 ...
PMID:Effects of staphylococcal enterotoxin B on rodent mast cells. 137 85

Semi-chronic exposure of ICR male Mice to Aflatoxin B1 (AFB1) in non-toxic doses results in elevated lung tryptophan (TRP) levels without change in serotonin (5-HT) or 5-hydroxyindole-3-acetic acid (5-HIAA) levels. This change is organ specific in that TRP levels are not altered in spleen, duodenum, heart or central nervous system (CNS). Acute (48 hour) flunixin treatment decreases lung TRP levels and reverses the AFB1 mediated increase in lung TRP levels. On the other hand, flunixin treatment decreases CNS TRP levels in control mice but not in AFB1 treated mice. Aflatoxin B1 treated mice have an increase in splenic serotonin (5-HT) content. Acute (48 hour) treatment of mice with E. coli lipopolysaccharide (LPS) also increases splenic 5-HT, and AFB1 treatment followed by LPS have a slightly additive effect on spleen 5-HT content. Treatment of mice with LPS increases heart 5-HT, an effect which is not altered in AFB1 pretreated mice. Both LPS and AFB1 per se increases lung TYR levels although the combination of treatments is not significantly different from the control value. Flunixin treatment increases lung tyrosine (TYR) levels, an effect which is not altered by AFB1 pretreatment. Acute treatment with either LPS or flunixin decreases the CNS TRP/TYR ratio; pretreatment with AFB1 prevents those changes in the CNS TRP/TYR ratio. Central nervous system catecholamines are reduced in AFB1 pretreated mice. However, CNS catecholamine changes in AFB1 treated mice are normalized by vitamin E supplementation during the treatment period.
 ...
PMID:Aflatoxin B1 alters central and systemic tryptophan and tyrosine metabolism: influence of immunomodulatory drugs. 190 75

Newcastle disease virus (NDV) administration to mice increased concentrations of plasma corticosterone, with a maximal effect at 8 h. This elevation of plasma corticosterone concentrations was not observed in hypophysectomized animals in which the completeness of the hypophysectomy was verified by functional tests. NDV administration consistently increased concentrations of free tryptophan in all brain regions examined (prefrontal cortex, hypothalamus, and brain stem). It also caused an activation of cerebral catecholamine and indoleamine metabolism as determined by measurement of the amines and their catabolites. 3-Methoxy,4-hydroxyphenylethyleneglycol (MHPG), the major catabolite of norepinephrine (NE), homovanillic acid (HVA), a major catabolite of dopamine (DA), and 5-hydroxyindoleacetic acid (5-HIAA), the major catabolite of serotonin (5-HT), were all increased in both hypothalamus and brain stem. Ratios of catabolites to the parent amine, considered to be an index of utilization of the neurotransmitters, were increased for NE, DA, and 5-HT in the hypothalamus and for DA and 5-HT in the brain stem. This pattern of changes resembles that observed following stressors such as footshock or restraint. There were also significant increases of tryptophan, HVA, dihydroxyphenylacetic acid (DOPAC), and 5-HIAA in hypophysectomized relative to sham-operated mice. The NDV treatment also increased thymus weights and markedly decreased the proliferative responses of isolated spleen cells to phytohemagglutinin, concanavalin A, pokeweed mitogen, and Escherichia coli lipopolysaccharide. These changes were not caused by increased circulating corticosterone because they were present at equal magnitude in hypophysectomized mice. Thymosin alpha 1 concentrations in the plasma were not altered by NDV or hypophysectomy. These results indicate that administration of NDV to mice can initiate neurochemical and endocrine responses like those observed during stress and can also cause immunosuppression. They are thus consistent with the hypothesis that a virus can be a stressor.
 ...
PMID:Effects of Newcastle disease virus administration to mice on the metabolism of cerebral biogenic amines, plasma corticosterone, and lymphocyte proliferation. 350 12

The effects of 5,7-dihydroxytryptamine (5,7-DHT) and 6-hydroxydopamine (6-OHDA) on the febrile response to E. coli lipopolysaccharide (LPS) of unanesthetized rats examined. Depleting serotonin (5-HT) in brain with 5,7-DHT produced an attenuation in fever response to LPS, while depleting noradrenaline (NA) content in the preoptic area with 6-OHDA produced an opposite effect. However, 6-OHDA when given intraventricularly (icv) was without any significant effect on fever response to LPS. Presented data indicate that alterations in both noradrenergic and serotoninergic system of the rat brain affect the febrile response response to bacterial pyrogen. Moreover, one might conclude that integrity of noradrenergic neurons in central nervous system (CNS) in the rat is not essential for appearance of pyrogen fever.
 ...
PMID:Effects of 5,7-dihydroxytryptamine and 6-hydroxydopamine on fever response in conscious rats. 732 44

In this study the effect of immune system stimulation and intracerebroventricular (i.c.v.) administration of interleukin-1 beta (IL-1 beta) on hippocampal serotonergic neurotransmission, behavioral activity, and the hypothalamic-pituitary-adrenocortical (HPA) axis is described. An in vivo microdialysis method was used to measure hippocampal extracellular concentrations of serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in conscious, freely moving rats. In addition, we established a method to continuously monitor free corticosterone levels in dialysates. Behavioral activity was scored by measuring the time during which rats were active (locomotion, grooming, eating, drinking). We found a significant, positive relationship between behavioral activity and hippocampal extracellular concentrations of 5-HT. Intraperitoneal (i.p.) administration of the bacterial endotoxin lipopolysaccharide (LPS; 30, 100, and 300 micrograms/kg body weight) produced an increase in the extracellular concentrations of 5-HT and 5-HIAA in the hippocampus, which was paralleled by a significant decline in behavioral activity and a marked increase in extracellular corticosterone levels. Thus, the close correlation between hippocampal extracellular 5-HT levels and behavioral activity observed in control rats was disrupted in the LPS-treated animals. The effects of i.p. LPS could be mimicked by i.c.v. application of recombinant human IL-1 beta (hIL-1 beta; 100 ng). i.c.v. pretreatment with the IL-1 receptor antagonist (IL-1ra; 10 micrograms) antagonized the hIL-1 beta-induced effects. IL-1ra showed no intrinsic effects. Furthermore, it was found that i.c.v. pretreatment with IL-1ra (10 micrograms) significantly attenuated the i.p. LPS-induced (100 micrograms/kg body weight) rise in hippocampal extracellular 5-HT levels.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of bacterial endotoxin and interleukin-1 beta on hippocampal serotonergic neurotransmission, behavioral activity, and free corticosterone levels: an in vivo microdialysis study. 753 23

Serotonin is a well-known neurotransmitter and neuroimmunomodulator which has been reported to modulate T cell and NK cell proliferation. In this study we investigated whether serotonin could regulate mitogen-stimulated proliferation of the mature B lymphocyte. Mouse and rat spleen cells were cultured with serotonin in the presence or absence of a combination of Escherichia coli lipopolysaccharide and dextran sulfate, and proliferation was assessed by [3H]thymidine uptake or propidium iodide staining of DNA. Serotonin alone had no effect on spleen cell proliferation, while it increased mitogen-stimulated B cell proliferation in a dose- and time-dependent manner. These effects were reproduced by the selective 5-HT1A receptor agonist 8-OH-DPAT. Serotonin- or 8-OH-DPAT-induced increase in proliferation could be blocked by the 5-HT1A receptor antagonists (+)WAY 100135 and propranolol. Moreover, lipopolysaccharide-activated mouse spleen cells expressed specific binding sites for [3H]8-OH-DPAT. These results show that serotonin upregulates mitogen-stimulated B lymphocyte proliferation through 5-HT1A receptors, thus providing an important link between this neurotransmitter and the immune system.
 ...
PMID:Serotonin upregulates mitogen-stimulated B lymphocyte proliferation through 5-HT1A receptors. 775 18

Previous studies have shown that the production of interstitial collagenase by rat myometrial smooth muscle cells is dependent on serotonin. These cells fail to produce collagenase early in culture, however, and produce the enzyme only 8-12 days after confluence. During the early quiescent period, collagenase production can be induced by low concentrations of bacterial endotoxin. Under these conditions, interleukin (IL)-1 alpha and IL-1 beta mRNAs increase coincident with collagenase and collagenase mRNA. Serotonin removal decreases IL-1 alpha and IL-1 beta mRNAs, and effect that is rapidly reversed upon readdition of serotonin. Conversely, serotonin-dependent increases in IL-1 mRNAs are blocked by progesterone. Experiments with 5-HT2 receptor agonists and antagonists indicate that induction is mediated by the 5-HT2 receptor subtype. In serotonin-treated cells late in culture, IL-1 mRNAs increase coincident with the production of collagenase. Similarly, exogenous IL-1 fully substitutes for lipopolysaccharide in stimulating myometrial cells to produce collagenase early in culture. Cells treated with IL-1 receptor antagonist fail to make IL-1 mRNAs or collagenase but produce collagenase and IL-1 mRNAs following antagonist removal. These results indicate that serotonin-dependent IL-1 production by the myometrial cell is required for collagenase production and that IL-1 participates in its own production via an autocrine mechanism.
 ...
PMID:Serotonin regulation of interleukin-1 messenger RNA in rat uterine smooth muscle cells. Relationship to the production of interstitial collagenase. 796 54

The effect of endotoxic lipopolysaccharide (LPS) on platelet shape change (PSC; a preaggregation event) was investigated. PSC is accompanied by an increase in median platelet volume (MPV), which was measured using a channelyzer. In whole blood, but not in platelet rich plasma (PRP), LPS (final concentration 80 mg/l) caused an increase in MPV that could be detected for 2 h. When PRP (prepared from LPS- and saline-pretreated whole blood) was incubated for 40 min, the LPS-mediated increase in MPV could no longer be detected. Taken together, these data imply that PSC is both initiated and maintained by a labile factor(s) present in whole blood, but not in PRP. PRP was prepared from LPS-pretreated whole blood and incubated for 40 min to allow reversal of the LPS-induced PSC; further stimulation with LPS caused PSC. Platelets from LPS-pretreated whole blood also showed enhanced PSC with serotonin (5-HT), diminished PSC with platelet activating factor (PAF), and no change of response to ADP and collagen. Hence, LPS pretreatment of whole blood differentially alters responses of platelets to further stimulation with LPS and other agonists. A specific PAF antagonist completely abolished the effect of LPS on MPV. These data may contribute to an understanding of the cascading thrombotic events and thrombocytopenia associated with septicaemia.
 ...
PMID:Platelet shape change in whole blood: differential effects of endotoxin. 809 94

In this study, the effects of serotonin (5-HT) on in vitro lymphoproliferation in rainbow trout (Oncorhynchus mykiss) are investigated. Serotonin exerted immunosuppressive effects on lipopolysaccharide (LPS) and phytohemagglutinin (PHA)-stimulated proliferation of fish peripheral blood lymphocytes (PBL). 8-OH-DPAT (an agonist of 5-HT1A receptors) mimicked the inhibitory effects of serotonin on lymphocyte proliferation, whereas addition of spiperone (an antagonist of 5-HT1A and 5-HT1B receptors) reversed these inhibitory effects, indicating that 5-HT1A receptors may be implicated in serotonin-induced immunosuppression. Furthermore, in this study the serotonergic receptors present on fish peripheral lymphocytes were characterized. A Scatchard plot of serotonin binding to fish lymphocytes followed the 'bell' shape curve with a Bmax of 0.63 microM and a Kd of 1.54 x 10(-8) M/10(6) cells. These results demonstrate the presence of positive-type co-operation among receptor populations. In a displacement study, serotonin inhibited the binding of 3H-5HT to the receptor sites both in resting and LPS/PHA-stimulated trout lymphocytes. Interestingly, the agonists (8-OH-DPAT and buspirone) and antagonist (NAN-190) of the 5-HT1A receptor subtype failed to displace 3H-5HT binding to receptor sites in resting cells, whereas these agents inhibited 3H-5HT binding in LPS- and PHA-stimulated lymphocytes significantly, suggesting that after mitogenic stimulation, 5-HT1A receptors are expressed on lymphocytes. CGS-12066B (an agonist of 5-HT1B receptors) failed to influence significantly 3H-5HT binding to receptor sites both in resting and mitogen-stimulated lymphocytes, indicating that the 5-HT receptor subpopulation is not expressed either on resting or on LPS- or PHA-stimulated lymphocytes. Taken together, these results suggest that trout peripheral blood lymphocytes express functional serotonergic receptors, and 5-HT1A receptors, which are not expressed by resting lymphocytes, are expressed after mitogenic stimulation and implicated in the inhibition of mitogenic (LPS and PHA) responses.
 ...
PMID:Serotonin modulation of lymphocyte proliferation via 5-HT1A receptors in rainbow trout (Oncorhynchus mykiss). 891 29


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