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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although a number of studies indicate that the pyrogenic activity of lipopolysaccharide (LPS) and/or interleukin (IL)-1 is mediated via induction of IL-6, this has been questioned by recent evidence demonstrating a dissociation between fever and circulating IL-6. The present study reexamines this relationship by use of human recombinant interleukin-1 receptor antagonist (IL-1ra). Injection of LPS (100 micrograms/kg ip) into rats induced fever (2.0 degrees C) that was significantly inhibited (P < 0.05) when IL-1ra (16 mg/kg ip) was given 1 and 2 h after LPS. The rise in plasma IL-6 preceded the febrile response by 1-1.5 h and, although the concentrations of bioactive IL-6 in plasma and cerebrospinal fluid (CSF) were not reduced at 4 h, at 2 h plasma and CSF IL-6 bioactivity was inhibited by 80 and 70%, respectively, after a single injection of IL-1ra (16 mg/kg ip). Intracerebroventricular injection of IL-1ra (200 micrograms/rat) inhibited LPS fever but did not affect the plasma IL-6 bioactivity measured 2 or 4 h after intraperitoneal LPS. These data show that peripheral IL-1 plays a part in the induction of both fever and the rise in plasma IL-6 that precedes it, and that IL-1 within the brain is also important in the induction of fever by LPS.
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PMID:Interleukin-1 receptor antagonist inhibits endotoxin fever and systemic interleukin-6 induction in the rat. 877 79

The involvement of interleukin-1 in antidipsogenic effects induced by intraperitoneal (i.p.) administration of lipopolysaccharide (0.32, 0.64 and 0.96 mg/kg) in 24-h water-deprived rats, was evaluated by injection of human interleukin-1 receptor antagonist (10, 25 and 50 micrograms/rat) into the lateral cerebral ventricle (i.c.v.). The effects of either lipopolysacharide or human interleukin-1 receptor antagonist treatment on rectal temperature of 24-h water-deprived rats, were examined. Our date show that human interleukin-1 receptor antagonist administration is able to reverse, dose dependently, fever, but not lipopolysaccharide inhibition of thirst. The reduction of pyrogenic, but not of antidipsogenic, effects of lipopolysaccharide following human interleukin-1 receptor antagonist administration suggests that lipopolysaccharide inhibition of thirst is not dependent on interleukin-1 induced fever and that interleukin-1 is not a direct mediator implicated in inhibition of water intake provoked by peripheral injection of lipopolysaccharide.
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PMID:Interleukin-1 receptor antagonist does not reverse lipopolysaccharide-induced inhibition of water intake in rat. 887 44

Intracerebroventricular (i.c.v.) interleukin-10 (25, 50, and 100 ng/rat) effects on water intake, exploratory behaviour, and rectal temperature were evaluated in rats treated intraperitoneally (i.p.) with lipopolysaccharide (0.32, 0.64, and 0.96 mg/kg). Endotoxin administration induced fever and inhibition of thirst in water-deprived rats, and a decrease in lococomotory activity in normohydrated and water-deprived animals. Our data show that interleukin-10 during lipopolysaccharide administration controlled fever, increases exploratory behaviour, but did not reverse lipopolysaccharide inhibition of thirst. These effects suggest that fever, depression in locomotory activity but not inhibition of thirst, induced by endotoxin are influenced by interleukin-10 levels.
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PMID:Effects of interleukin-10 on water intake, locomotory activity, and rectal temperature in rat treated with endotoxin. 922 77

Alveolar macrophage and type II cells are known to generate nitric oxide, which is a highly reactive molecule that plays a role in host defense against pathogens, as well as tissue damage associated with inflammation in the lung. Both types of cells are known to generate the nitric oxide by inducible nitric oxide synthase (iNOS). Surfactant-associated protein A (SP-A) from various sources (human alveolar proteinosis, rat and recombinant rat) was found to upregulate nitric oxide production by alveolar macrophages in a concentration- and time-dependent manner, whereas type II cells were unresponsive to SP-A. The increase in nitric oxide production was associated with elevation in the expression of iNOS. However, only 30-50% of the cells responded by expressing iNOS, as was observed by immunofluorescence staining. The stimulatory effect of SP-A was found to be 30-50% lower than the known nitric oxide agonists interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS). However, addition of the cytokines interleukin-1 or granulocyte macrophage colony-stimulating factor elevated the levels of nitric oxide production to that of LPS and IFN-gamma. Special attention was given to exclude the possibility that contaminating LPS in the various SP-A species stimulated nitric oxide production by the macrophages. Our results indicate that SP-A is the agonist and not a contaminating LPS. The data presented in this report extend our knowledge regarding the nonsurfactant-related functions of SP-A.
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PMID:Nitric oxide production by rat alveolar macrophages can be modulated in vitro by surfactant protein A. 922 23

To examine the effect of Helicobacter pylori lipopolysaccharide on gastric secretion, the present study was carried out using pylorus ligated conscious rats. Intraperitoneal administration of Helicobacter pylori lipopolysaccharide significantly inhibited gastric acid secretion (4 hr) in a dose-dependent manner (0.033-1.0 mg/rat). The Helicobacter pylori lipopolysaccharide (1 mg/rat)-induced acid inhibition was still observed 8 hr after injection. Gastric acid secretion (4 hr) was compared in the rats that had received intraperitoneal administration of 1 mg/rat dose of Helicobacter pylori lipopolysaccharide or saline alone 24 hr before. There was no significant difference in gastric acid secretion between the saline- and H. pylori lipopolysaccharide-treated rats. These results suggest for the first time that H. pylori lipopolysaccharide may inhibit acid production, and this acid inhibition may be long-lasting. It is also demonstrated that this anti-secretory action of H. pylori lipopolysaccharide has a reversible effect on gastric secretion. All these results suggest that H. pylori lipopolysaccharide might be involved in the low acid secretory function seen in patients with acute H. pylori infection.
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PMID:Helicobacter pylori lipopolysaccharide inhibits acid secretion in pylorus-ligated conscious rats. 924 Apr 75

Activation of the immune system by lipopolysaccharide (LPS) produces physiological, neuroendocrine and behavioral effects, some of which are mediated by cytokine production. We have previously shown that the cytokine interleukin-1 (IL-1) inhibits sexual behavior in female, but not male rats, while producing a comparable suppression of locomotion in both sexes. The present study examined the effects of LPS on sexual behavior and locomotion of male and female rats, and the involvement of IL-1 receptors in mediating the effects of IL-1 and LPS on females' behavior. Peripheral (i.p.) administration of LPS (50 or 250 microg/kg) significantly decreased sexual behavior in females, up to 6 h after administration, while it had no effect on male sexual behavior. However, locomotor activity, measured in the open-field test, was similarly reduced by LPS in both males and females. Pretreatment with the IL-1 receptor antagonist (IL-1ra) either i.p. (10 mg/kg) or intracerebroventricularly (i.c.v.) (50 microg/rat) did not prevent the inhibition of female sexual behavior and locomotion induced by either i.p. (50 microg/kg) or i.c.v. (200 or 400 ng/rat) administration of LPS, respectively. However, identical doses of IL-1ra significantly reversed the effects of IL-1beta, administered either i.p. (5 microg/kg) or i.c.v. (50 ng/rat), respectively. These results demonstrate that both LPS and IL-1beta produce marked inhibition of sexual behavior in female, but not in male rats. However, IL-1 receptors are not required for the effects of LPS on sexual behavior in female rats.
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PMID:Different receptor mechanisms mediate the effects of endotoxin and interleukin-1 on female sexual behavior. 940 16

To study the role of the sympathetic nervous system in the induction of inflammatory cytokines elicited by central lipopolysaccharide, sympathetic chemical denervation was performed by intraperitoneal injection of 6-hydroxydopamine. Rats received the neurotoxin according to the following schedule: 50 mg/kg on days 1 and 2, 100 mg/kg on days 3, 4 and 7. On day 8, lipopolysaccharide (2.5 microg/6 microl/rat) was injected intracerebroventricularly and rats were killed 2 h later. 6-Hydroxydopamine reduced noradrenaline and dopamine content in the spleen by 88.7% and 88.8% respectively, without affecting striatal contents indicating that the chemical sympathectomy had been effective and selective. In sympathectomized rats, lipopolysaccharide raised interleukin-1beta and interleukin-6 serum levels more than in control rats given the vehicle. Tumour necrosis factor-alpha serum levels in sympathectomized rats were no different from those in vehicle-treated rats. Interleukin-1beta and interleukin-6 messenger RNA expression, measured by northern blot analysis, was clearly detectable in adrenals and spleen of rats given lipopolysaccharide. Sympathectomy increased lipopolysaccharide-induced interleukin-1beta and interleukin-6 messenger RNA in adrenals and spleen. Corticosterone basal levels were raised by central lipopolysaccharide and not further changed by sympathectomy. The present study shows that sympathetic nervous system denervation enhances the synthesis and production of peripheral interleukin-1beta and interleukin-6 in rats given central lipopolysaccharide and suggests a tonic inhibitory control of the sympathetic nervous system on these inflammatory cytokines.
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PMID:The sympathetic nervous system tonically inhibits peripheral interleukin-1beta and interleukin-6 induction by central lipopolysaccharide. 950 62

Bacterial lipopolysaccharide (LPS) or endotoxin induces neurological manifestations including anorexia. It is proposed that LPS-induced cytokine production is involved in the generation of neurological manifestations and in neuroinflammatory/immunological responses during gram-negative infections. For example, LPS-induced effects can be blocked or ameliorated by the interleukin-1 receptor antagonist (IL-1Ra). Here, sensitive and specific RNase protection assays were used to investigate the effects of the intracerebroventricular (i.c.v.) administration of LPS on mRNA levels of interleukin-1beta (IL-1beta) system components, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, and neuropeptide Y (NPY) in the cerebellum, hippocampus, and hypothalamus. The same brain region sample was analyzed with all of the antisense probes. The data show simultaneous local induction of multiple cytokine components messenger ribonucleic acids (mRNAs) within specific brain regions in anorectic rats responding to i.c.v. administered LPS (500 ng/rat). Interleukin-1beta and IL-1Ra had a similar mRNA induction profile (hypothalamus > cerebellum > hippocampus). Interleukin-1 receptor type I (IL-1RI) mRNA also increased in all three brain regions examined, and the soluble form of IL-1 receptor accessory protein (IL-1R AcP II) mRNA was induced in the hypothalamus. Tumor necrosis factor-alpha mRNA levels increased in the hypothalamus > hippocampus > cerebellum. Levels of membrane bound IL-1R AcP, TGF-beta1, and NPY mRNAs did not change significantly in any brain region. The results suggest that: (1) endogenous up-regulation of IL-1beta and TNF-alpha in the hypothalamus contribute to LPS-induced anorexia; and (2) the ratio IL-1Ra/IL-1beta, and IL-1beta <--> TNF-alpha interactions may have implications for gram-negative infections associated with high levels of LPS in the brain-cerebrospinal fluid.
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PMID:Interleukin-1beta system (ligand, receptor type I, receptor accessory protein and receptor antagonist), TNF-alpha, TGF-beta1 and neuropeptide Y mRNAs in specific brain regions during bacterial LPS-induced anorexia. 957 Jul 21

Inflammatory cytokines may mediate the host response to infection via central nervous system, endocrine, and/or paracrine/autocrine signaling mechanisms. Previous studies have shown that intravenous administration of interleukin (IL)-1 beta alters the concentration of the anabolic hormone insulin-like growth factor (IGF)-I in plasma and various tissues. The purpose of the present study was to determine 1) whether the intracerebroventricular injection of IL-1 beta can influence peripheral IGF-I levels in control animals and 2) whether the central administration of a IL-1 receptor antagonist (IL-1ra) can prevent the changes in peripheral IGF-I induced by endotoxin [lipopolysaccharide (LPS)] or sepsis produced by cecal ligation and puncture. In the first experiment, injection of IL-1 beta (100 ng/rat) decreased IGF-I levels in plasma, liver, and gastrocnemius muscle 28-36% by 1.5 h in conscious fasted rats. IGF-I levels remained reduced at 3 h, but returned to baseline by 6 h. IGF-I content was not altered in soleus, kidney, spleen, intestine, or whole brain after IL-1 beta. In the second series of experiments, LPS injected intravenously decreased IGF-I levels in plasma, liver, and gastrocnemius at 1.5 h, and levels were even further reduced at 3 and 6 h in these tissues (59, 57, and 48%, respectively). Moreover, the IGF-I content was also decreased in soleus (30-35%) and increased in kidney (2- to 3-fold) after LPS. In the third experiment, changes in IGF-I levels in plasma and tissues, similar to those seen in LPS-treated rats, were detected 24 h after induction of peritonitis. Intracerebroventricular infusion of IL-1ra did not alter any of the changes in IGF-I produced by either LPS or sepsis, although it did attenuate the concomitant changes in growth hormone levels. These data suggest that, although central IL-1 beta is capable of modulating peripheral IGF-I levels, central administration of IL-1ra was unable to modulate the changes in peripheral IGF-I in blood and tissues produced by either endotoxemia or peritonitis.
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PMID:Role of central IL-1 in regulating peripheral IGF-I during endotoxemia and sepsis. 957 56

This study investigated the effects of lipopolysaccharide (LPS) and interleukin-1beta (IL-1beta) on corticotropin releasing factor (CRF) and prostaglandin E2 (PGE2) release by brainstem slices in vitro. First, we characterized our experimental model and demonstrated that high potassium stimulates CRF release from rat brainstem slices in a calcium dependent way. The direct stimulation of brainstem slices with IL-1beta (3-25 pM) did not modify basal or potassium-stimulated CRF release, although IL-1beta at the dose of 25 pM increased PGE2 production. Peripheral injection (i.p.) of LPS (1-10 microg/kg) or IL-1beta (1-10 microg/kg) evoked a dose-related potentiation of the ex-vivo release of CRF and PGE2 from brainstem slices. However, central (i.c.v.) administration of LPS (10-500 ng/rat) potentiated the release of CRF and PGE2 only at the dose of 500 ng/rat, whereas IL-1beta (1-100 ng/rat) failed to modify significantly the ex vivo production of both CRF and PGE2. The results of the present study provide evidence that peripheral, rather than central, endotoxin and IL-1beta administration induce the activation of brainstem CRF and PGE2, supporting the hypothesis that peripheral cytokine signalling to the CNS is mediated by stimulation of peripheral afferents.
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PMID:Effect of endotoxin and interleukin-1beta on corticotropin-releasing-factor and prostaglandin release by rat brainstem slices. 968 45


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