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)

Several immunological abnormalities were detected in the cerebrospinal fluid (CSF) of human immunodeficiency virus type 1 (HIV-1)-infected children. Intrathecal synthesis of immunoglobulins, free light chains (FLC), IL-1 beta, IL-6, and M-CSF were demonstrated both in asymptomatic children and children with subacute encephalopathy. Our findings further support the hypothesis that an immunopathological subclinical process within the central nervous system (CNS) may be an early manifestation of acquired immunodeficiency syndrome (AIDS). Cytokine detection in the CSF may represent a useful diagnostic tool in evaluating the outcome of HIV-1-infected patients.
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PMID:Immunological markers in the cerebrospinal fluid of HIV-1-infected children. 186 84

Immunological and viral studies were conducted on cerebrospinal fluid from 31 HIV-1-infected children, of whom 23 were neurologically asymptomatic and 8 had progressive encephalopathy. After AZT treatment, a second cerebrospinal fluid specimen was obtained from 15 children, 11 of whom were neurologically asymptomatic and 4 had progressive encephalopathy. Virus isolation and p24Ag detection were more frequent in children with progressive encephalopathy than in asymptomatic children (66% versus 12%) and were inversely correlated with intrathecal HIV-1-antibody detection (anti-gag AB: 25% versus 70%). High concentrations of interleukin-1 beta (IL-1 beta) and IL-6 were found in children with progressive encephalopathy (50% and 37%, respectively), but low levels were also detected in some asymptomatic children (13% and 9%, respectively). Tumour necrosis factor-alpha (TNF alpha) was not found. AZT treatment induced disappearance of p24Ag in cerebrospinal fluid, as well as a marked reduction in cytokine levels. Cytokine determination may be useful in monitoring AZT treatment in children with progressive encephalopathy.
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PMID:Cerebrospinal fluid analysis in HIV-1-infected children: immunological and virological findings before and after AZT therapy. 784 99

Human immunodeficiency virus infection leads to a deregulated production of a number of cytokines. Some of them (IL-1, IL-6, TNF-alpha, interferon-gamma) are produced in increased amounts in vivo, whereas the production of IL-2 is decreased. This latter abnormality plays a pivotal role in the establishment of the immunodeficiency. Some cytokines (IL-1, IL-6, TNF-alpha) stimulate the in vitro replication of HIV, whereas others (mainly the interferons) inhibit it. The effect of cytokines in vivo in the spreading of HIV remains, however, largely unknown. Cytokines may also be involved in the development of many clinical manifestations associated with HIV infection. IL-1, IL-6 and TNF-alpha may play a role in tissue damages associated with opportunistic infections, in HIV-related encephalopathy and in cachexia. Cytokines, mainly IL-6, IL-10 and IL-13, may stimulate the growth of malignant cells during Kaposi sarcoma or lymphomas. Better knowledge of the role of cytokines during HIV infection should allow new therapeutic approaches based on the use of either recombinant cytokines or specific antagonists, with the aim of limiting both HIV spreading and the clinical manifestations of this infection.
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PMID:Cytokines in HIV infection. 792 84

Monocytes/macrophages play a critical role in the pathogenesis of HIV infection, both as targets for virus replication and as sources of production of multifunctional cytokines. Endothelins, peptides with potent vasoconstricting activities originally isolated from endothelial cells, are also produced and secreted by macrophages in a manner similar to that of other cytokines. In an attempt to explore the potential role of endothelins in HIV-infection, we investigated the effect of the HIV-1 envelope glycoprotein, glycoprotein 120, on monocytic endothelin-1 production. This glycoprotein has been identified as a potent stimulator of monokines such as TNF-alpha and IL-6, which have been implicated as potential mediators of HIV-encephalopathy. We found that glycoprotein 120, similar to LPS, stimulates the secretion of endothelin-1, as well as TNF-alpha, from macrophages in a concentration-dependent manner. Using reverse transcriptase polymerase chain reaction, we found that circulating monocytes in HIV-infected individuals show a distinct expression of the endothelin-1 gene that is not detectable in healthy controls, indicating chronic activation of this gene in HIV-infection. In addition, cerebral macrophages in patients with HIV-encephalopathy were strongly positive for endothelin. Thus, monocytic endothelins appear to be stimulated during HIV infection. Their potent vasoactive properties render them potential candidates for mediating alterations in the cerebral perfusion pattern associated with the AIDS dementia complex.
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PMID:Potent stimulation of monocytic endothelin-1 production by HIV-1 glycoprotein 120. 848 49

In the literature the separation between RS and RLS is confusing and makes it difficult to plan an appropriate preventive action or to develop new therapeutic approaches. We suggest that the generalized damage and encephalopathy seen in both RS and RLS may be due to a wide variety of causative agents that contribute to a common derangement, principally involving mitochondrial oxidative pathway. Fasting status and infections increase the catabolism and the subsequent flux of metabolites from peripheral tissues to the liver (FA and amino acids); cytokines (TNF, IL-1, and IL-6), in particular, mediate this effect during infection and experimental endotoxemia. Some drugs and other toxic compounds induce functional and morphological liver mitochondrial derangement. Oxidative metabolism is impaired, with subsequent stimulation of alternative pathways of oxidation, following production of unusual toxic acyl CoAs and dicarboxylic acids. Toxic compounds accumulate in the liver, deranging its functions and causing energy depletion, and are also released in the circulation from which they reach other tissues, including the brain. Neurons and astrocytes in the brain may be affected differently: Neurons suffer from the lack of energy and the effect of toxic compounds arriving from the bloodstream, and astrocytes may be directly affected by the beta-oxidation derangement. Very important may be genetic predisposition, which, by making the patient more sensitive to a particular causative agent, may facilitate the onset of RS and RLS. The therapeutic approach is, presently, mainly symptomatic, directed as it is to counteracting each alteration shown, depending by the clinical gravity. Other pharmacological approaches are only studied experimentally, like carnitine supplementation and PGE2 administration, or theoretically envisaged, like monoclonal antibody therapy directed at LPS or at pro-inflammatory cytokines or treatment with interferon-alpha.
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PMID:Reye's and Reye-like syndromes, drug-related diseases? (causative agents, etiology, pathogenesis, and therapeutic approaches). 852 53

The capacity of two human fetal glial cell lines, SVG and POJ, to increase the expression of human immunodeficiency virus (HIV) was investigated. As a cellular model for HIV latency, a chronically infected promonocytic cell line U1 was used. This cell line constitutively expresses a low level of viral activity. To monitor the level of HIV expression in U1 cells, reverse transcriptase (RT) activity was measured in the supernatant and the level of total HIV proteins was determined in cellular lysates. It was observed that the conditioned media from SVG and POJ cells increased RT activity in U1 cells in a dose-dependent fashion. In addition, the conditioned media from fetal glial cells caused an increase in total HIV protein synthesis. The capacity of conditioned media from both fetal glial cell lines to induce the expression of HIV was reduced by 45% in the presence of antibodies against human tumor necrosis factor alpha (TNFalpha), suggesting that one of the HIV-activating factors released by these cells was TNFalpha. The presence of TNFalpha and two other HIV-activating cytokines, IL-6 and IL-1, was confirmed by ELISA. It was also observed that glutathione increased the HIV-inducing capacity of the fetal glial cell-derived conditioned media. The finding that fetal glial cells constitutively secrete soluble factors which increase the expression of HIV in vitro suggests that in vivo, during perinatally acquired infection, similar events may occur. Fetal glial cells may play an important role in the pathogenesis of HIV-related encephalopathy.
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PMID:Human fetal glial cells constitutively produce HIV-inducing cytokines. 860 23

The neuropathology associated with HIV (Human Immunodeficiency Virus) infection is one of the major complications of this disease. The virological and cellular mechanisms by which HIV infection induces motor and cognitive disorders remain unknown. This lack of understanding of the pathophysiology is partly due to the difficulty of experimental analysis in man because only post-mortem samples from terminal phases of the disease and cerebrospinal fluid samples are available. Two animal models, very closely resembling human HIV infection, are available: the cat model infected by FIV (Feline Immunodeficiency Virus) and the macaque model infected by the SIVmac (Simian Immunodeficiency Virus) which have enabled us to conduct a longitudinal study of encephalopathy during primo-infection and the asymptomatic and pre-AIDS (Acquired Immune Deficiency Syndrome) phases. In the cat-FIV model, which presents the advantage of being non-infectious to man, and therefore easier to manipulate, it was shown that infected cats develop behavioural abnormalities and a neuropathology which resemble HIV dementia. Central nervous system lesions induced by FIV are similar to those of HIV infection apart from the absence of multinucleated giant cells. This model was used to analyse the relationship between CNS lesions and the viral load of the brain and showed that the severity of the lesions contrasted with a low viral load. The pathophysiology of SIVmac infection in the rhesus macaque is almost identical to human infection with a more rapid course, since the duration of the asymptomatic phase is 6 months to 5 years, depending on the animal. We studied the relationship between lesions, viral load and cytokine production (IL-1 beta, IL-2, IL-6, TNF alpha, INF gamma, TGF-beta 1) within the CNS. Our results show early, low-grade and constant infection of the brain. The dissociation between the viral load and the lesions observed is our favour of an indirect mechanism for the pathogenesis of these lesions. The relationship between lesions and the cytokine profile studied shows the importance of glial cells in the pathogenesis of the lesions.
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PMID:[Contribution of animal models in the understanding of AIDS encephalopathy]. 938 13

We investigated the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 alpha (IL-1 beta), and IL-6 as proinflammatory cytokines in CSF to facilitate differentiation between acute encephalitis/encephalopathy and prolonged febrile seizures. We studied 20 children with prolonged febrile seizures and 23 with acute encephalitis/encephalopathy, including 8 with an acellular CSF. TNF-alpha, IL-1 beta, and IL-6 in CSF were measured by ELISA. We found that TNF-alpha, IL-1 beta, and IL-6 were undetectable in CSF of all children with prolonged febrile seizures and control subjects but that the concentrations of TNF-alpha was elevated in 11, of IL-1 alpha in 6, and of IL-6 in 17 of 23 children with acute encephalitis/encephalopathy. Twenty-two of 23 children with acute encephalitis/encephalopathy had elevated concentrations of one or more cytokine. Elevated concentrations of the CSF proinflammatory cytokines, TNF-alpha, IL-1 beta, and IL-6, indicate acute encephalitis/encephalopathy rather than febrile seizures.
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PMID:Tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 in cerebrospinal fluid from children with prolonged febrile seizures. Comparison with acute encephalitis/encephalopathy. 948 63

Parenteral injection of endotoxin has been used as a model to examine the role of pro-inflammatory cytokines in the centrally controlled responses to Gram-negative bacterial infection. However, the events that occur following mucosal exposure to live bacteria have received little attention. In this study, we have used a murine model to demonstrate that respiratory infection with Bordetella pertussis, which is associated with a number of systemic complications including fever, seizure and encephalopathy in children, resulted in persistent expression of mRNA transcripts for IL-1beta and TNFalpha and transient expression of IL-6 in the hippocampus and hypothalamus. These changes correlated with elevated levels of cytokine protein in the same brain areas. The results demonstrate that infection at a mucosal surface can result in the induction of pro-inflammatory cytokine production in the brain and suggest that these locally synthesized mediators may contribute to the centrally controlled clinical manifestations of B. pertussis infection.
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PMID:Induction of inflammatory cytokines in the brain following respiratory infection with Bordetella pertussis. 1063 86

CT/MRI findings, laboratory examinations and prognoses of 42 patients with acute encephalopathy (AE) (Japan Coma Scale > or = 200) were reported. 1. Findings on CT/MRI were divided into the following 7 categories: Group 1 (normal), Group 2 (CT/MRI looked normal in acute phase, but brain atrophy developed and progressed slowly by weeks or months), Group 3 (CT/MRI looked normal within a few days after the onset of AE, but cortical laminar necrosis developed at 4-5 days after the onset), Group 4 (marked brain edema developed within 2 days after the onset of AE), Group 5 (AE with symmetric thalamic lesions), Group 6 (symmetric pallidum, lesions on MRI which appeared after brain edema disappeared), and Group 7 (the brain shrinked during acute phase, which normalized on the follow up CT/MRI). 2. Serum AST elevated in approximately 50% of the patients with AE. Sixty percent of them exhibited DIC, whose prognoses were poor. Cerebrospinal fluids (CSF) neopterin (NP) and/or interleukin (IL)-6 were elevated in all the 8 patients examined. In the two cases whose serum NP and IL-6 were measured at the same time, their values in the CSF were higher than those in the serum in one case, and almost the same in the other. In a patient with a condition mimicking hemorrhagic shock and encephalopathy, serum IL-6 concentration was very high (94,000 pg/ml). 3. Mild hypothermia (around 34 degrees C) combined with methylprednisolone pulse therapy was excellently effective on AE. A 6-year-old boy exhibited tonsillar herniation at admission recovered well to be able to run. 4. Differentiation between Reye syndrome and HSE, and the pathogenesis of AE were also discussed.
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PMID:[Infection-related acute encephalopathy: CT scan/MRI finding, laboratory examination and prognosis]. 1072 91


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