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

Blue-green algae toxins include (1) hepatotoxic peptides that are known to be toxic to cattle, dogs, swine, waterfowl, and sometimes other species; (2) a nicotinic agonist neurotoxin that appears to be toxic to a wide range of animal species; (3) a peripheral-acting cholinesterase inhibitor that is very toxic to swine, birds, and dogs; (4) toxins that impair nervous transmission by blocking sodium channels in nerve cells; and (5) lipopolysaccharide endotoxins. This article provides current information on the mechanisms of action of the primary toxins recognized to date as well as on procedures important in the diagnosis and management of some of the more common cyanobacterial toxicoses in livestock and waterfowl.
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PMID:Algae intoxication in livestock and waterfowl. 250 41

The time course of immunosuppression induced by acute treatment with O,O,S-trimethyl phosphorothioate (OOS-TMP), an impurity in technical formulations of malathion, was examined in female C57B1/6 mice. Both cell-mediated and humoral immune responses were examined and included allospecific cytotoxic T cells, proliferative response to mitogens, interleukin-2 production and antibody production to sheep red blood cells. OOS-TMP pretreatment led to a reversible suppression of the generation of cytotoxic T lymphocytes and antibody-secreting cells to sheep erythrocytes. However, the mitogenic response of splenocytes from animals treated with nontoxic doses of OOS-TMP (as measured by body weight loss, serum cholinesterase levels and splenic lymphocyte number) to concanavalin A was not significantly suppressed, but the response to the B cell mitogen lipopolysaccharide was slightly decreased on day 1 following treatment. In contrast, interleukin-2 production was elevated by 24 h following treatment, but had returned to control levels by day 7. These data suggest that OOS-TMP was able to block the generation of cytotoxic T lymphocytes and antibody responses at doses of OOS-TMP that did not affect body weight or splenic lymphocyte number and this suppression was reversible.
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PMID:Organophosphorus pesticide immunotoxicity: effects of O,O,S-trimethyl phosphorothioate on cellular and humoral immune response systems. 349 28

To evaluate the cause of the vulnerability to infections in the elderly, the ability of neutrophil to generate reactive oxygen species was assessed by a luminol-dependent chemiluminescence (CL) assay after stimulation with non-opsonized zymosan, Staphylococcus aureus, Pseudomonas aeruginosa, Klebsiella pneumoniae, Candida albicans and lumispheres in elderly patients aged 70 to 93 years. The integrated CL for 20 minutes of whole blood and neutrophils induced by zymosan in the elderly was significantly lower than that in healthy young adults, and the integrated CL of neutrophils induced by lumispheres was also significantly lower in the elderly aged 80 years and over. When bacterial infection occurred in the elderly, the levels of CL were elevated and decreased in the convalescence. This response is proper for host-defense mechanism against infection. However, whole blood CL response was not fully activated in any patients of the elderly during bacterial infection. In these cases lower white blood cell counts, lower neutrophil counts, or the decreased level of the serum total protein, albumin, total cholesterol or cholinesterase were observed. Relationship between malnutrition and the ability of neutrophil to generate reactive oxygen species was suggested. Furthermore, I evaluated the priming effect of lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) on whole blood CL. The CL responses stimulated with non-opsonized zymosan or P. aeruginosa were enhanced by pretreatment with TNF-alpha and LPS in healthy young adults. On the other hand, no significant priming effect was observed when blood from elderly patients were incubated with each primer. These findings suggest that the impairment in the generation of reactive oxygen species of the neutrophils and the decrease in reactivity to LPS and TNF-alpha that activate neutrophils at the site of infection and potentiate host defense against invading bacteria, may contribute to susceptibility to infection in the elderly.
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PMID:[Study of neutrophil dysfunctions in the elderly using a chemiluminescence method]. 782 5

Administration of lipopolysaccharide (LPS) at 3 mg/kg, i.p. in rats resulted in reduced food intake, febrile hyperthermia, decreased body weight and reduced muscle performance in treadmill tests. It also induced some biochemical changes like increased serum levels of transaminases, acid phosphatase, pseudocholinesterase, free fatty acids and decreased blood glucose and liver glycogen levels. Rhinax (RHX), a herbal formulation, at 160 mg/kg, p.o. improved muscle performance but had no effect on the elevated temperature or the reduced body weight of rats weakened by LPS. It also normalised various biochemical alterations induced by LPS. The results of these studies indicate efficacy of RHX as an antifatigue agent to improve muscular performance.
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PMID:Effect of rhinax on bacterial lipopolysaccharide induced endotoxemia in rats. 975 66

Oral chlorpyrifos (CHP) induces hypothermia followed by a fever that persists for several days in the rat. To understand the neuro-immune mechanisms of CHP-induced fever, we compared the tolerance and cross-tolerance between CHP and the fever elicited by lipopolysaccharide (LPS) (Escherichia coli). Female rats were administered the corn oil (CO) vehicle or CHP (10 mg/kg; p.o.) daily for 4 days while core temperature (Tc) and motor activity (MA) were monitored by telemetry. There was a reduction in Tc followed by an elevation the next day after each CHP treatment. The day after the last CHP treatment, rats were administered saline or 50 microg/kg LPS (i.p.). CHP-treated rats had a smaller LPS fever that was attributed to their elevated baseline Tc. In another study, rats were dosed with saline or LPS daily for three days. By the time of the third LPS injection there was no febrile response, indicating tolerance to LPS. Rats were then dosed with CO or CHP (10 mg/kg) 24 h after the third LPS treatment. LPS-tolerant rats displayed an accentuated hypothermic and febrile response to CHP. Plasma cholinesterase activity was unaffected by repeated LPS treatment, suggesting that the metabolism of CHP in the liver was unaffected by LPS. Overall, the neural-immune mechanisms for LPS fever is distinct from that of CHP in view of marked difference in mechanisms of tolerance.
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PMID:Delayed febrile effects of chlorpyrifos: is there cross-tolerance to bacterial lipopolysaccharide? 984 93

Oral exposure to chlorpyrifos (CHP) in the rat results in an initial hypothermic response followed by a delayed fever. Fever from infection is mediated by the release of cytokines, including interleukin-6 (IL-6) and tumor necrosis factor (TNF alpha). This study determined if the CHP-induced fever involves cytokine-mediated mechanisms similar to that of infectious fevers. Long-Evans rats were gavaged with the corn oil vehicle or CHP (10-50 mg/kg). The rats were euthanized and blood collected at various times that corresponded with the hypothermic and febrile effects of CHP. Plasma IL-6, TNF alpha, cholinesterase activity (ChE), total iron, unsaturated iron binding capacity (UIBC), and zinc were measured. ChE activity was reduced by approximately 50% 4 h after CHP. There was no effect of CHP on IL-6 when measured during the period of CHP-induced hypothermia or fever. TNF alpha levels nearly doubled in female rats 48 h after 25 mg/kg CHP. The changes in plasma cytokine levels following CHP were relatively small when compared to > 1000-fold increase in IL-6 and > 10-fold rise in TNF alpha following lipopolysaccharide (E. coli; 50 microg/kg; i.p.)-induced fever. This does not preclude a role of cytokines in CHP-induced fever. Nonetheless, the data suggest that the delayed fever from CHP is unique, involving mechanisms other than TNF alpha and IL-6 release into the circulation characteristic of infectious fevers.
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PMID:Are circulating cytokines interleukin-6 and tumor necrosis factor alpha involved in chlorpyrifos-induced fever? 1041 84

Inflammation has been recently implicated in pathogenesis of dementia disorders. Effect of anti-dementia (Acetylcholinesterase inhibitor) drugs tacrine, rivastigmine and donepezil were studied on neuroinflammation induced by intraperitoneal administration of lipopolysaccharide (LPS) in mice. Interleukin-2 (IL-2) and isoforms of acetylcholinesterase (AChE) were estimated in different brain areas as marker for neuroinflammation and cholinergic activity respectively. LPS significantly increased the level of IL-2 in all the brain areas while enhancement of AChE activity varied in brain areas. It was found that administration of tacrine, rivastigmine and donepezil in mice significantly attenuated the LPS induced increased levels of IL-2 along with the significant reduction of AChE activity predominantly in salt soluble (SS) fraction as compared to the detergent soluble (DS) fraction in a dose dependent manner. In vitro effect of LPS was also studied in different brain areas. LPS significantly increased the AChE activity in SS fractions but the significant increase was not found in DS fractions. The present study indicate that cholinesterase inhibitor anti-dementia drugs are effective against LPS induced neuroinflammation that may be linked to enhanced cholinergic activity.
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PMID:Effect of anti-dementia drugs on LPS induced neuroinflammation in mice. 1739 11

The present study was planned to investigate the effect of anti-cholinesterase drugs donepezil and neostigmine on neuroinflammation induced by intracerebroventricular administration of lipopolysaccharide (LPS, 50 microg) in rat. Proinflammatory cytokines (TNF-alpha and IL-1beta), expressions of iNOS and COX-2, acetylcholinesterase activity, malondialdehyde and reduced glutathione were studied in different brain regions at 24h of LPS injection. Donepezil was found to decrease the LPS-induced AChE activity and oxidative stress in all the brain regions. It also inhibited the LPS-induced proinflammatory cytokines and iNOS expression but did not affect the increased COX-2 expression whereas neostigmine treatment had no effect on LPS-induced proinflammatory cytokines. Methyllycaconitine (MLA), a alpha7 nicotinic acetylcholine receptor antagonist, significantly antagonized the donepezil mediated inhibition of LPS-induced proinflammatory cytokines, indicating that alpha7 nicotinic acetylcholine receptor subunit was playing a role in regulation of neuroinflammation. The phosphorylation of Akt, an effector of PI3K, increased with donepezil treatment. These results suggest that increased cholinergic activity in brain by donepezil prevents LPS-induced neuroinflammation via alpha7-nAChRs, followed by the PI3K-Akt pathway and this system may form the basis for the development of novel agents for reversing neuroinflammation or provide new indications for existing drugs.
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PMID:Cholinergic protection via alpha7 nicotinic acetylcholine receptors and PI3K-Akt pathway in LPS-induced neuroinflammation. 1978 87

Oral cocaine administration results in hepatic necrosis, increased plasma transaminase concentration, and decreased antioxidative capability, which is potentiated by lipopolysaccharide (LPS) in male CF-1 mice. Females administered the same treatment regimen display none of the hepatotoxic effects seen in their male counterparts. This study was conducted to further dissect the mechanism responsible for this gender difference in cocaine hepatotoxicity (CH) and lipopolysaccharide potentiation of CH. Male and female CF-1 mice were orally administered 20 mg/kg cocaine hydrochloride once daily for 7 days. Four hours after the last cocaine administration the mice were administered 12 x 10(6) EU LPS intraperitoneally. The activity of plasma esterase (butyrylcholinesterase), the enzyme responsible for the major pathway of cocaine metabolism to nonhepatotoxic metabolites, was measured. Aminotransferase release and histological analysis were used to determine hepatotoxicity. The concentration of the hepatotoxic precursor norcocaine was measured in the plasma and liver. Regardless of treatment, males were shown to have only 30% of the plasma esterase activity displayed by females. In addition, administration of testosterone to ovariectomized females resulted in a 70% reduction in plasma esterase activity when compared with surgically unaltered females. Moreover, hepatic norcocaine was not detected in the plasma or liver of surgically unaltered female animals, while it was present in males and testosterone-supplemented ovariectomized females. These results indicate that plasma esterase activity is heavily influenced by sex hormones, predominantly testosterone, in CF-1 mice. Suppression of plasma esterase by testosterone correlates with decreased norcocaine production and is therefore responsible, in part, for the increased CH seen following oral administration with and without LPS exposure in male CF-1 mice.
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PMID:Plasma butyrylcholinesterase activity protects against cocaine hepatotoxicity in female mice. 2002 Oct 60

The present study describes for the first time the in vitro properties (inhibition of NO production and anticholinesterase) of Phagnalon saxatile (L.) Cass. (Asteraceae). The methanolic extract showed antioxidant activity that was measured by DPPH assay and beta-carotene bleaching test. The same extract inhibited NO production in the murine monocytic macrophage cell line RAW 264.7. Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inhibition was assessed by modifications of Ellman's method. Purification of the MeOH extract of P. saxatile allowed the isolation of phenolic compounds. Among them, the compounds that most effectively inhibited lipopolysaccharide-induced NO production were caffeic acid and methylchlorogenic acid, with IC50 values of 7 microg/mL and 12 microg/mL, respectively. Luteolin and 3,5-dicaffeoylquinic acid exhibited the most promising activity against AChE with an IC50 of 25.2 and 54.5 microg/mL, respectively, while caffeic acid and luteolin exhibited higher activity against BChE with an IC50 of 32.2 and 37.2 microg/mL, respectively.
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PMID:Metabolite profile and in vitro activities of Phagnalon saxatile (L.) Cass. relevant to treatment of Alzheimer's disease. 2003 May 14


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