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)

This paper evaluates the current information on the relationship between oral disease (specifically periodontitis) and atherosclerosis/coronary heart disease (CHD) to determine whether the information is sufficient to conclude that periodontitis is a risk factor for atherosclerosis/CHD. As background for this evaluation, the term "risk factor" is defined, and the 3 criteria used to establish exposures as risk factors are reviewed. In addition, epidemiologic criteria for defining an exposure as causal are presented. The available evidence then is evaluated according to the criteria for causality, which are extensions of the criteria for establishing a risk factor. This review is done in the context of the relationship between atherosclerosis/CHD and inflammation. A number of findings are briefly reviewed that link inflammation and atherosclerosis/CHD, such as: 1) prior flu-like symptoms were more common in cases of myocardial infarction than in concurrently sampled controls; 2) high levels of cytomegalovirus antibody titers were associated with elevated carotid intimal-medial wall thickness 18 years later; 3) prior infection with cytomegalovirus was a strong independent risk factor for restenosis after coronary atherectomy; 4) dental infections were more common in cases of cerebral infarction compared to community controls matched on age and sex; and 5) the gingival index was significantly correlated with fibrinogen and white cell counts in periodontal patients and controls, adjusted for age, smoking, and socioeconomic status. Three case-control studies and 5 longitudinal studies investigating the relationship between dental conditions and atherosclerosis/CHD are reviewed in terms of strength of associations, consistency of associations, specificity. of associations, time sequence between exposure and outcome, and degree of exposure and outcome. Related to the last criterion, new findings are presented which indicate that the extent of the periodontal infection, a measure reflecting microbial burden, also is related to onset of new CHD events. Our previously published model describing the potential biological mechanisms underlying the associations found is reviewed. This model places the associations into a context of an intrinsic or acquired hyperinflammatory monocyte trait that results in a more intense inflammatory response to lipopolysaccharide (LPS) challenges, such as periodontal infections. This hyperinflammatory response may promote atheroma formation and thromboembolic events. finally, new findings from ongoing animal studies are presented, indicating that high fat diets in atherosclerotic-susceptible mice induce greater inflammatory responses to Porphyromonas gingivalis challenges. We conclude that the available evidence does allow an interpretation of periodontitis being a risk factor for atherosclerosis/CHD. This conclusion, however. is made with some qualifications. While the associations found across a wide variety of subjects are remarkably consistent, for the most part they are represented by incidence odds ratios around 2.0. While this level of association would result in oral conditions contributing to a large number of CHD cases, it is possible that associations of this magnitude are due to bias in the study designs. In addition, some studies report that periodontitis is associated with all-cause mortality and low birth weight infants. These multiple associations detract from the credibility of periodontitis as a risk factor, as specificity of association is more often related to causality. However, all-cause mortality may largely be driven by mortality from cardiovascular events: and some exposures, such as smoking. are indeed risk factors for multiple conditions. On the other hand, current findings regarding the associations between oral conditions and atherosclerosis/CHD imply that the criteria for causality may be met in the not-too-distant future.
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PMID:Periodontitis: a risk factor for coronary heart disease? 972 97

Epidemiological studies show a markedly increased risk of cerebral palsy following the combined exposure of infection and birth asphyxia. However, the underlying mechanisms of this increased vulnerability remain unclear. We have examined the effects of a low dose of bacterial endotoxin on hypoxic--ischaemic injury in the immature brain of rats. Bacterial endotoxin (lipopolysaccharide 0.3 mg/kg) was administered to 7-day-old rats 4 h prior to unilateral hypoxia--ischaemia and the neurological outcome was determined 3 days later. Rectal temperature and cerebral blood flow was measured during the study and the expression of CD14 and toll-like receptor-4 mRNA in the brain was examined. We found that a low dose of endotoxin dramatically sensitizes the immature brain to injury and induces cerebral infarction in response to short periods of hypoxia--ischaemia that by themselves caused no or little injury. This effect could not be explained by a reduction in cerebral blood flow or hyperthermia. In association with the sensitization of injury we found an altered expression of CD14 mRNA and toll-like receptor-4 mRNA in the brain. These results suggest that the innate immune system may be involved in the vulnerability of the immature brain following the combination of infection and hypoxia--ischaemia.
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PMID:Bacterial endotoxin sensitizes the immature brain to hypoxic--ischaemic injury. 1128 7

Yuldahansotang (YH-Tang), a Sasang Constitutional prescription composed of seven herbal mixtures, has been developed as a formula to prevent and treat cerebral infarction (CI) of Taeumins. However, the mechanisms by which this formula affects CI remain unknown. Previously, regulation of serum cytokine levels by YH-Tang has been observed in individuals at the acute stage of CI disease. It is uncertain whether this is a cause or a result of the disease process. In this study, we investigated whether YH-Tang inhibited secretion of inflammatory cytokines from human astrocytes. YH-Tang regulated the cytokine secretions in astrocytes stimulated with substance P (SP) and lipopolysaccharide (LPS). YH-Tang significantly inhibited interleukin (IL)-1, IL-4, IL-6 and tumor necrosis factor-alpha (TNF-alpha) secretion in astrocytes stimulated with SP and LPS, but did not inhibit interferon-y (IFN-gamma) and IL-2 secretion significantly. IL-1 has been shown to elevate TNF-alpha secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. Therefore, we investigated whether IL-1 mediated inhibition of TNF-alpha secretion from astrocytes by YH-Tang. Incubation of human astrocytes with IL-1 antibody abolished the synergistic cooperative effect of LPS and SP. These results suggest that YH-Tang may indirectly inhibit TNF-alpha secretion by inhibiting IL-1 secretion. Moreover, these findings indicate that YH-Tang has regulatory effects on cytokine secretion in an acute CI patient.
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PMID:Cytokine production regulation in human astrocytes by a herbal combination (Yuldahansotang). 1202 45

Thioredoxin (Trx) is a small redox-active protein with antioxidant and antiapoptotic effects. Trx transgenic (Tg) mice are more resistant to cerebral infarction and survive longer than wild-type (WT) C57BL/6 mice. The aim of the present study was to investigate the protective role of Trx in acute hepatitis models. The expression of endogenous Trx was decreased in thioacetamide (TAA)-induced acute hepatitis. TAA (100 microg/g) was injected intraperitoneally in WT and Tg mice. Survival rate after TAA injection was higher in Tg mice than in WT mice. The level of oxidative stress was significantly less in Tg mice than in WT mice, as shown by the protein carbonylation assay and lipid peroxidation assay. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive cells were less in Tg mice than in WT mice, which was consistent with DNA laddering assay. Caspase-3 and caspase-9 activities and cytochrome c release were significantly inhibited in Tg mice compared with those in WT mice. In addition, lipopolysaccharide (LPS) plus d-galactosamine (GalN), or anti-Fas antibody (Jo2) were injected. Survival rate after LPS plus GalN injection was much higher in Tg mice than in WT mice. In contrast, there was no difference in survival rate after Jo2 injection between WT and Tg mice. In conclusion, transgene of Trx attenuated TAA- or LPS-induced acute lethal hepatitis. In addition to an antioxidant effect, Trx has the potential to protect acute liver injury via an antiapoptotic effect, which mainly inhibits mitochondria-mediated apoptosis signaling.
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PMID:Overexpression of thioredoxin prevents acute hepatitis caused by thioacetamide or lipopolysaccharide in mice. 1271 82

Interleukin-1 (IL-1) has pleiotropic actions in the central nervous system. During the last decade, a growing corpus of evidence has indicated an important role of this cytokine in the development of brain damage following cerebral ischemia. The expression of IL-1 in the brain is dramatically increased during the early and chronic stage of infarction. The IL-1 gene cluster on chromosome 2q14 contains three related genes (IL1alpha, IL1beta, and IL1 receptor antagonist) located within a 430-kb region. T and C alleles exist for the IL-1alpha-889 regulatory region and the TT genotype has been reported to increase the production of the protein in lipopolysaccharide (LPS)-stimulated mononuclear cells from IL-1alpha-889 TT carriers. We examined whether the IL-1alpha polymorphism affects the probability of cerebral infarction (CI). We genotyped 360 CI patients and 519 healthy controls for the same polymorphism. A significant increase was found for the IL-1alpha T allele in CI patients compared with controls (chi2=5.026, P=0.025). We conclude that the IL-1alpha-889 polymorphism is a major risk factor for CI in Koreans.
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PMID:Association of interleukin-1 alpha gene polymorphism with cerebral infarction. 1282 54

The herbal formulation "Jeo Dang-Tang" (JDT) has long been used for various cerebrovascular diseases. However, very little has scientific investigation been carried out. The aim of the present study is to investigate the effect of JDT on the production of various cytokines in the patients with cerebral infarction (CI). Peripheral blood mononuclear cells (PBMC) obtained from the patients with CI were cultured for 24h in the presence or absence of lipopolysaccharide (LPS) or phytohemagglutinin (PHA). The amount of interleukin (IL)-4, IL-10 and transforming growth factor (TGF)-1beta, in culture supernatant, was significantly increased in the JDT, LPS or PHA treated cells compared to unstimulated cells (P < 0.05). We also show that increased IL-4, and IL-10 level by LPS or PHA was significantly inhibited by JDT in a dose-dependent manner. Maximal inhibition rate of IL-4 and IL-10 production by JDT was 45 +/- 2% and 51 +/- 5% for LPS-stimulated cell and 41.5 +/- 3% and 70.8 +/- 2% for PHA-stimulated cells, respectively (P < 0.05). On the other hand, JDT significantly increased the LPS or PHA-induced TGF-beta1 production (P < 0.05). These data suggest that JDT has a regulatory effect on the cytokines production, which might explain its beneficial effect in the treatment of CI.
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PMID:The effect of Jeo Dang-Tang on cytokines production in the patients with cerebral infarction. 1468 93

Seogak Jihwang-Tang (SJT) has been widely used to treat patients suffering from cerebral infarction. However, very little scientific investigation has been carried out. We investigated the effect of SJT on the production of various cytokines using peripheral blood mononuclear cells from the cerebral infarction patients presenting with altered consciousness. The cytokines production was determined by enzyme-linked immunosorbent assay. The amount of IL-4, IL-10 and TGF-beta1 in culture supernatant significantly increased in the SJT, lipopolysaccharide (LPS) or PHA-treated cells compared to unstimulated cells (P < 0.05). We also showed that increased IL-4 and IL-10 levels by LPS or phytohaemagglutinin (PHA) were significantly inhibited by SJT in a dose-dependent manner. Maximal inhibition rate of IL-4 and IL-10 production by SJT was 45.6 +/- 3.3% and 61 +/- 4.7% for LPS-stimulated cells and 27.3 +/- 1.2% and 83.6 +/- 2% for PHA-stimulated cells, respectively (P < 0.05). On the other hand, SJT significantly increased the LPS or PHA-induced TGF-beta1 production (P < 0.05). These data suggest that SJT has a regulatory effect on the cytokines production, which might explain its beneficial effect in the treatment of cerebral infarction.
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PMID:Differential regulation by Seogak Jihwang-Tang on cytokines production in peripheral blood mononuclear cells from the cerebral infarction patients presenting with altered consciousness. 1532 33

Peroxisome proliferator-activated receptor gamma (PPAR-gamma) is a nuclear membrane-associated transcription factor that governs the expression of various inflammatory genes. PPAR-gamma agonists protect peripheral organs from ischemic injury. In the present study, we investigated whether the PPAR-gamma agonist rosiglitazone is neuroprotective against focal ischemic brain injury. C57/B6 mice underwent 1.5-h middle cerebral artery occlusion, and received either vehicle or rosiglitazone treatment of 0.75, 1.5, 3, 6 or 12 mg/kg (n = 9 per group). Cerebral infarct volume, neurological function, expression of pro-inflammatory proteins and neutrophil accumulation were assessed after ischemia and reperfusion. At 48 h after ischemia, infarct volume was significantly decreased with 3-12 mg/kg of rosiglitazone, with a time window of efficacy of 2 h after ischemia at the optimal dose (6 mg/kg). Neutrophil accumulation was significantly decreased in the brain parenchyma of rosiglitazone-treated mice. Ischemia-induced expression of several inflammatory cytokines and chemokines was markedly reduced in rosiglitazone-treated brains, as determined using proteomic-array analysis. Rosiglitazone treatment improved neurological function at 7 days after ischemia. Moreover, in cultured cortical primary microglia, rosiglitazone attenuated inflammatory responses by decreasing lipopolysaccharide-induced release of tumor necrosis factor-alpha, interleukin (IL)-1beta and IL-6. These results suggest that the PPAR-gamma agonist rosiglitazone has neuroprotective properties that are at least partially mediated via anti-inflammatory actions, and is thus a potential novel therapeutic agent for stroke.
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PMID:Neuroprotection against focal ischemic brain injury by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone. 1653 67

Yangkyuk-Sanhwa-Tang (YST) has been used for the Soyangin cerebral infarction (CI) patients according to Sasang constitutional philosophy. This study investigated the effect of YST on production of various cytokines using peripheral blood mononuclear cells (PBMCs) from the Soyangin CI patients group. The amount of interleukin (IL)-1alpha, IL-1beta, IL-6, IL-8, and tumor necrosis factor-alpha increased in the lipopolysaccharide (LPS)-treated cells compared with unstimulated-cells. YST inhibited IL-1alpha, IL-1beta, and IL-8 production in PBMCs stimulated with LPS. These data suggest that YST has a regulatory effect on cytokine production, which might explain its beneficial effect in the treatment of Soyangin CI patients.
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PMID:Inhibitory effect of Yangkyuk-Sanhwa-Tang on inflammatory cytokine production in peripheral blood mononuclear cells from the cerebral infarction patients. 1736 33

Yulda-Hanso-Tang (YHT) has been used as a formula for the cerebral infarction (CI) patients. This study investigated the anti-inflammatory effects and possible mechanism of YHT on lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells. The amount of interleukin-1beta, IL-4, IL-6, IL-8, and tumor necrosis factor-alpha was increased in the LPS-treated cells. But, increased cytokine was inhibited by YHT except IL-8. The study showed that YHT inhibited the IL-1beta mRNA expression. YHT also inhibited LPS-induced activation of NF-kappaB and degradation of IkappaBalpha. These results suggest that YHT is an inhibitor of NF-kappaB, which might explain its beneficial effect in the treatment of inflammatory diseases.
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PMID:Yulda-Hanso-Tang attenuates the endotoxin-induced inflammatory cytokine production in peripheral blood mononuclear cells. 1761 18


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