Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effectiveness of plasma exchange (PE) with continuous hemodiafiltration (CHDF) in the treatment of critically ill patients was evaluated based on changes in cytokine levels. Twenty-six patients with acute hepatic failure were treated with PE (PE group) or PE and CHDF (PE+CHDF group), and the levels of cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-8 were determined before and after treatment. Bilirubin levels were significantly lower after treatment in both the PE and PE+CHDF groups. There were no significant differences in TNF-alpha levels before and after treatment in the PE group, but the TNF-alpha level was significantly lower after treatment in the PE+CHDF group. There were no significant differences in the IL-6 levels before and after treatment in both the PE and PE+CHDF groups. There were no significant differences in IL-8 levels before and after treatment in the PE group, but the IL-8 level was significantly lower after treatment in the PE+CHDF group. PE with CHDF therapy was given to 5 patients with acutely aggravated autoimmune diseases, 2 patients with hemorrhagic shock and encephalopathy syndrome, and 3 patients with thrombotic microangiopathy. The results suggested that PE with CHDF therapy are useful in critically ill patients with suspected hypercytokinemia.
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PMID:Cytokine removal by plasma exchange with continuous hemodiafiltration in critically ill patients. 1246 Apr 4

In this report we describe pertussis toxin-induced reversible encephalopathy dependent on monocyte chemoattractant protein-1 (MCP-1) overexpression (PREMO), a novel animal model that exhibits features of human encephalopathic complications of inflammatory disorders such as viral meningoencephalitis and Lyme neuroborreliosis as well as the mild toxic encephalopathy that commonly precedes relapses of multiple sclerosis (MS). Overexpression of the mouse MCP-1 gene product (classically termed JE) in astrocytes, the major physiological CNS cellular source of MCP-1, failed to induce neurological impairment. Unexpectedly, transgenic (tg) mice overexpressing MCP-1 at a high level (MCP-1(hi)) manifested transient, severe encephalopathy with high mortality after injections of pertussis toxin (PTx) plus complete Freund's adjuvant (CFA). Surviving mice showed markedly improved function and did not relapse during a prolonged period of observation. Tg mice that expressed lower levels of MCP-1 were affected minimally after CFA/PTx injections, and tg expression of other chemokines failed to elicit this disorder. The disorder was significantly milder in mice lacking T-cells, which therefore play a deleterious role in this encephalopathic process. Disruption of CC chemokine receptor 2 (CCR2) abolished both CNS inflammation and encephalopathy, identifying CCR2 as a relevant receptor for this disorder. Proinflammatory and type 1 cytokines including TNF-alpha, IL-1beta, IFN-gamma, IL-2, RANTES, and IP-10 were elevated in CNS tissues from mice with PREMO. These studies characterize a novel model of reversible inflammatory encephalopathy that is dependent on both genetic and environmental factors.
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PMID:Pertussis toxin-induced reversible encephalopathy dependent on monocyte chemoattractant protein-1 overexpression in mice. 1248 56

Recently, the number of reports of encephalopathy associated with influenza has increased in Japan. The abrupt onset of seizure and coma after development of high-grade fever is a prominent indicator of CNS involvement. Approximately 600 patients have been reported during 1999-2002. 78% of them are younger than 6 yr old, and the mortality was 30% in 1999 and 2000 seasons. The pathogenicity of brain dysfunction is still unknown. However, elevation of cytokines(TNF-alpha and IL-6) and the damage of vascular endothelial cells were demonstrated. Thus, the prognosis of this illness was extremely poor. Intensive care trial in combination with (1) anti-virals, (2) high dose gamma-grobulin, (3) steroid pulse therapy. (4) high dose AT III, (5) head cooling and (6) plasma exchange has started since 2001, that could reduce the mortality from 30 to 15% in 2001 and 02. In order to establish more effective treatment, further investigation will be necessary.
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PMID:[Treatment of influenza-associated encephalopathy]. 1461 46

The tumor necrosis factor (TNF-alpha) is a cytokine known as a mediator of inflammation and immunity. The genes coding the tumor necrosis factors alpha and beta are considered part of class III major histocompatability complex. The 2 involved genes have been mapped to chromosome 6. Certain mutations in the TNF-alpha gene are believed to be causative for increased production of the cytokine. In this respect, the most common variant is the TNF2 allele, a single nucleotide substitution of guanine by adenine at position -308 relative to the promoter transcription site of the gene. Elevated production of TNF-alpha has been found to be associated with several infectious diseases including malaria. Elevated levels of TNF-alpha have also been observed to associate with increased risk of preterm delivery, chorioamnionitis and fetal morbidity including encephalopathy. The present article reviews the genetics of the cytokine TNF-alpha and discusses its suitability as a candidate marker for assessment of increased risk of preterm delivery and fetal morbidity.
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PMID:The cytokine TNF-alpha. Genetics and suitability for prenatal risks assessment. 1496 5

The neuropathological correlates of encephalopathy and autonomic dysfunction in septic shock are unclear. We performed post mortem analysis of 5 brain areas susceptible to ischemia and 5 autonomic nuclei (AN) in 23 patients who had died in our intensive care unit (ICU) from septic shock and 8 dying from non-septic shock as well as 5 controls who had died suddenly from extracranial injury. Proinflammatory cytokine (IL1-beta and TNF-alpha) and inducible nitric oxide synthase (iNOS) expression was assessed by immunocytochemistry. Abnormalities in septic shock were: hemorrhages (26%), hypercoagulability syndrome (9%), micro-abscesses (9%), multifocal necrotizing leukoencephalopathy (9%) and ischemia (100%). The incidence of cerebral hemorrhage or hypercoagulability syndrome was not related to clotting disturbances. The intensity of ischemia within susceptible areas was the same in both ICU groups, but more pronounced in the autonomic centers of septic patients (P < 0.0001). Neuronal apoptosis assessed using anti-caspase 3 immunocytochemistry and in situ end labeling was more pronounced in the autonomic nuclei of septic patients. (P < 0.0001). TNF-alpha expression did not differ between groups but vascular iNOS expression assessed by immunocytochemistry was higher in sepsis (P<0.0001) and correlated with autonomic center neuronal apoptosis (P < 0.02). We conclude that septic shock is associated with diffuse cerebral damage and specific autonomic neuronal apoptosis which may be due to circulating factors particularly iNOS.
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PMID:The neuropathology of septic shock. 1499 34

Liver transplantation, considered today as the most effective treatment for end-stage liver diseases, can not always be performed on every patient affected with a liver disease. Patients with end-stage liver diseases, usually have high bilirubin, encephalopathy and renal failure. In these situations cytokines play an important role in different processes, from apoptosis to regeneration. The aim of this clinical study has been to analyse the action of new artificial liver system, called Molecular Adsorbent Recycling System (MARS) on cytokines metabolism in patients affected with acute on chronic liver failure. The results are intriguing because an increase of IL-6 and a decrease of TNF-alpha observed during MARS treatment. The study confirms the efficacy of MARS therapy in terms of homeostasis of the cytokines network and suggests an usefulness of monitoring their level during liver failure.
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PMID:Cytokines and liver failure: modification of TNF- and IL-6 in patients with acute on chronic liver decompensation treated with Molecular Adsorbent Recycling System (MARS). 1505 25

Dengue virus encephalopathy was experimentally induced in newborn mice by i.p. inoculation of dengue 2 virus. At 6 and 9 days post-infection, motor incoordination and posterior limb paralysis were observed with focal necrosis, apoptotic cells, perivascular inflammatory cuffing and astrocytosis, mainly in the cortex and hippocampus. Expression of dengue virus genome and mRNA encoding for TNF-alpha, IL-1alpha, IL-2, IL-6, IL-1beta, IL-12 p40, IFNalpha, and IFNbeta; in addition host survival and inflammatory response genes MAC-1, EB22, GFAP, ICAM-1 and A20, were increased, suggesting that experimental dengue encephalitis could be associated with virus replication, inflammatory cytokine production or both. Similar findings have been observed in human dengue virus infection. Therefore, our results can be useful to elucidate and support the physiopathology of the disease.
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PMID:Cytokine production in brain of mice experimentally infected with dengue virus. 1510 28

In hyperbilirubinemic newborns, sepsis is considered a risk factor for kernicterus. Evidence shows that injury to astrocytes triggers cytokine release. We examined the effects of unconjugated bilirubin (UCB) alone, or in combination with LPS, on the release of glutamate and cytokines from astrocytes in conditions inducing less than 10% of cell death. UCB leads to an increase of extracellular glutamate and highly enhances the release of TNF-alpha and IL-1beta, while inhibiting the production of IL-6. LPS potentiates immunostimulatory properties of UCB. These results point out the role of cytokines and provide a basis for the significance of sepsis in UCB encephalopathy.
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PMID:Cytokine production, glutamate release and cell death in rat cultured astrocytes treated with unconjugated bilirubin and LPS. 1526 64

In term neonatal encephalopathy, little is known about the relationship between early inflammatory markers, neonatal brain injury, and long-term neurodevelopmental outcome. Our goal was to determine whether neonatal serum cytokine levels are associated with cerebral metabolism assessed by proton magnetic resonance spectroscopy (MRS), with magnetic resonance imaging (MRI) abnormalities, and with neurodevelopmental outcome at 30 mo of age. Levels of seven cytokines [IL-1 beta, IL-6, IL-8, IL-9, IL-12, IL-13, and tumor necrosis factor (TNF)-alpha] were measured in dried neonatal blood by immunoaffinity chromatography in a prospective cohort of 62 term newborns at risk of neonatal encephalopathy. MR images (n = 61) were scored and lactate/choline and N-acetyl-aspartate (NAA)/choline were measured by MRS (n = 42) on median day of life 6 in the deep gray nuclei (DGN) and in the watershed/cortical zone (WS). Neurodevelopmental outcome (n = 54) was considered abnormal if the infant died or if cognitive delay and/or functional motor deficit were detected at 30 mo. IL-1 beta, IL-6, IL-8 and TNF-alpha were significantly associated with lactate/choline in the DGN (p = 0.03, 0.02, 0.03, and 0.01 respectively), but not in the WS (all p > 0.1). Cytokines were not associated with NAA/choline in any region or with MRI scores. Children with abnormal neurodevelopmental outcome had higher neonatal levels of IL-1 beta, IL-6, IL-8, and lower levels of IL-12 (p = 0.04, 0.03, 0.01, 0.03 respectively). Elevated inflammatory cytokines were associated with impaired cerebral oxidative metabolism, but not with detectable MRI changes in the neonatal period. Understanding the link between elevated cytokines and outcome would inform novel strategies of cerebral protection.
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PMID:Neonatal encephalopathy: association of cytokines with MR spectroscopy and outcome. 1549 11

Microglia are the resident immune cells of the brain and are the principal source of cytokines produced during central nervous system inflammation. We have previously shown that increased levels of unconjugated bilirubin (UCB), which can be detrimental to the central nervous system during neonatal life, induce the secretion of inflammatory cytokines and glutamate by astrocytes. Nevertheless, the effect of UCB on microglia has never been investigated. Hence, the main goal of the present study was to evaluate whether UCB leads to microglial activation and to the release of the cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. Additionally, we investigated the effects of UCB on glutamate efflux and cell death. The results showed that UCB induces morphological changes characteristic of activated microglia and the release of high levels of TNF-alpha, IL-1beta, and IL-6 in a concentration-dependent manner. In addition, UCB triggered extracellular accumulation of glutamate and an increased cell death by apoptosis and necrosis. These results demonstrate, for the first time, that UCB is toxic to microglial cells and point to microglia as an important target of UCB in the central nervous system. Moreover, they suggest that UCB-induced cytokine production, by mediating cell injury, can further contribute to exacerbate neurototoxicity. Interestingly, microglia cells are much more responsive to UCB than astrocytes. Collectively, these data indicate that microglia may play an important role in the pathogenesis of encephalopathy during severe hyperbilirubinemia.
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PMID:Unconjugated bilirubin activates and damages microglia. 1661 33


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