Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reverse transcriptase-dependent polymerase chain reaction (RT-PCR) was applied to the detection and differentiation of viral hemorrhagic septicemia virus (VHSV) and infectious hematopoietic necrosis virus (IHNV) using primer pairs designed for the amplification of glycoprotein G-specific gene fragments of the two viruses. The products of 443 bp (VHS) and 548 bp (IHN), respectively, were amplified from the total RNA extracts of RTG-2 cells infected with a total of 9 different strains of either VHS virus or IHN virus. Restriction analysis using FokI, and DNA sequencing of the PCR products demonstrated specificity of the amplification. The RT-PCR amplification of VHSV or IHNV G-genes was found to be a simple, highly specific and sensitive method allowing differential diagnosis of VHS and IHN within 8 h.
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PMID:Differential diagnosis of fish pathogenic rhabdoviruses by reverse transcriptase-dependent polymerase chain reaction. 857 1

1. Induction of nitric oxide synthase (iNOS) results in overproduction of nitric oxide (NO), which may be a principal cause of the massive vasodilatation and hypotension observed in septic shock. Since NO-induced vasorelaxation is mediated via the soluble isoform of guanylate cyclase (sGC), the regulation of sGC activity during shock is of obvious importance, but yet poorly understood. The aim of the present study was to investigate the activation of sGC by sodium nitroprusside (SNP) before and after exposure of rat aortic smooth muscle cells to endotoxin (LPS) or interleukin-1 beta (IL-1 beta). 2. Exposure of rat aortic smooth muscle cells to SNP (10 microM) elicited up to 200 fold increases in cyclic GMP. This effect was attenuated by 30-70% in IL-1 beta- or LPS-pretreated cells, in a pretreatment time-and IL-1 beta- or LPS-concentration-dependent manner. When, however, cells were exposed to IL-1 beta or LPS and then stimulated with the particulate guanylate cyclase activator, atriopeptin II, no reduction in cyclic GMP accumulation was observed. 3. Pretreatment of rats with LPS (5 mg kg-1, i.v.) for 6 h led to a decrease in aortic ring SNP-induced cyclic GMP accumulation. 4. The IL-1 beta-induced reduction in SNP-stimulated cyclic GMP accumulation in cultured cells was dependent on NO production, as arginine depletion abolished the downregulation of cyclic GMP accumulation in response to SNP. 5. Reverse-transcriptase-polymerase chain reaction analysis revealed that the ratio of steady state mRNA for the alpha, subunit of sGC to glyceraldehyde phosphate dehydrogenase was decreased in LPS- or IL-1 beta-treated cells, as compared to vehicle-treated cells. 6. Protein levels of the alpha 1 sGC subunit remained unaltered upon exposure to LPS or IL-1 beta, suggesting that the early decreased cyclic GMP accumulation in IL-1 beta- or LPS-pretreated cells was probably due to reduced sGC activation. Thus, the observed decreased responsiveness of sGC to NO stimulation following cytokine or LPS challenge may represent an important homeostatic mechanism to offset the extensive vasodilatation seen in sepsis.
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PMID:Downregulation of nitrovasodilator-induced cyclic GMP accumulation in cells exposed to endotoxin or interleukin-1 beta. 883 57

Recent studies suggest that interleukin-6 (IL-6) is produced in the intestinal mucosa during sepsis and endotoxemia and that the enterocyte may be a source of IL-6 in these conditions. The regulation of IL-6 production in the enterocyte is not fully understood. We tested the hypothesis that IL-6 production in the enterocyte is regulated by proinflammatory cytokines. This was done by treating cultured Caco-2 cells, a transformed human intestinal epithelial cell line, with different concentrations of tumor necrosis factor-alpha (TNF-alpha), IL-1 beta, IL-6 or interferon-gamma (IFN-gamma). IL-6 production by the Caco-2 cells was determined by ELISA. The expression of IL-6 mRNA was determined by reverse-transcriptase polymerase chain reaction. IL-6 was not produced in unstimulated Caco-2 cells. Treatment of the Caco-2 cells with IL-1 beta resulted in a dose- and time-dependent stimulation of IL-6 production with a maximal effect noted at an IL-1 beta concentration of .5 ng/mL at 24 h. IFN-gamma alone did not stimulate IL-6 production but potentiated the effect of IL-1 beta in a synergistic fashion. Treatment of the Caco-2 cells with IL-1 beta induced expression of IL-6 mRNA with a response noticed after 30 min. TNF-alpha and IL-6 did not influence the production of IL-6 in the Caco-2 cells. The results suggest that enterocyte IL-6 production is stimulated by IL-1 beta and that this effect is potentiated by IFN-gamma. The regulation of IL-6 production in the enterocyte may be specific for IL-1 beta, since neither TNF nor IL-6 stimulated IL-6 production.
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PMID:Interleukin-1 beta and interferon-gamma regulate interleukin-6 production in cultured human intestinal epithelial cells. 932 25

Interleukin-1 (IL-1) is a proinflammatory cytokine produced by blood-borne and resident inflammatory lung tissue involved in the thrombotic occlusion of the pulmonary microcirculation and the increase of the vascular permeability following a wide variety of injuries and sepsis. The locally accentuated, organ-related activation of this cytokine seems to be responsible for the development of acute lung injury. The present study was conducted to determine if IL-1beta was produced in an ischemia-reperfusion (I/R) rat model subjected to lung injury. We measured sequential perfusate levels of IL-1beta by ELISA and we measured IL-1 gene expression in the rat lung tissue by a reverse-transcriptase polymerase chain reaction method. Little IL-1beta gene expression was observed in normal rat lung tissue. Perfusate IL-1beta slightly increased 2 h after induced ischemia and 3 h after reperfusion. IL-1beta gene expression rapidly increased as early as 30 min after ischemia and continued to increase for up to 120 min. IL-1beta gene expression was dramatically upregulated during reperfusion after cessation of ischemia, reached a peak at 1 h, and then gradually decreased (2 to 3 h) to near baseline levels. During ischemia, the increased IL-1 gene expression was not significantly different between the ventral and dorsal sites of the lung. However, IL-1 gene expression markedly increased on the dorsal part (the dependent site for a rat in a supine position) after reperfusion. From these results, it appears that IL-1 may have an important role in I/R lung injury.
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PMID:Interleukin-1 in ischemia-reperfusion acute lung injury. 935 26

The complete nucleotide sequence of the fish rhabdovirus viral hemorrhagic septicemia virus (VHSV) has been determined. The genome comprises 11158 bases and contains six long open reading frames encoding the nucleoprotein N, phosphoprotein P, matrix protein M, glycoprotein G, nonstructural viral protein NV, and polymerase L. Genes are arranged in the order 3'-N-P-M-G-NV-L-5'. The exact 3' and 5' ends were determined after RNA-oligonucleotide ligation or RACE. They show inverse complementarity as in other rhabdovirus genomes. Nucleotide and deduced amino acid sequences exhibit significant homology to corresponding sequences in the related fish rhabdovirus infectious hematopoietic necrosis virus.
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PMID:Complete genomic sequence of viral hemorrhagic septicemia virus, a fish rhabdovirus. 1049 51

The effect of sepsis on the ubiquitously expressed ATP-sensitive potassium (uK(ATP)-1) channel expression was measured in Sprague-Dawley rat diaphragms. Rats were treated with either 0.5 ml saline or 20 mg/Kg E. coli lipopolysaccharides and sacrificed at 3, 6, 12, 24, or 48 h later. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that channel mRNA expression was increased at 3 h and continued to rise up to 48 h. Western blotting analysis showed a approximately 9-fold increase in channel protein expression 24 h after sepsis. Our results demonstrate that sepsis upregulates the uK(ATP)-1 channel.
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PMID:Induction of the ATP-sensitive potassium (uK(ATP)-1) channel by endotoxemia. 1084 76

Clinical and experimental studies have implicated high circulating levels of the cytokine tumour necrosis factor-alpha (TNF-alpha) in the pathogenesis of insulin resistance, not only in obesity and diabetes, but also in clinical conditions associated with cachexia and sepsis. TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. In addition, protein kinase C (PKC) has recently been implicated in the mechanism of TNF-alpha-induced insulin resistance. The present study investigated the effects of TNF-alpha and a PKC inhibitor (RO-318220) on basal and insulin-stimulated 2-[(3)H]deoxyglucose uptake in cultured L6 myoblasts. Reverse transcriptase-PCR analysis confirmed that L6 myoblasts express TNF-alpha receptors I and II (p60 and p80). Dose-response curves for glucose uptake were fitted to a quadratic function to derive C(I-150) values (concentration of insulin required to increase glucose uptake by 50%). Incubation with TNF-alpha at 1 or 10 ng/ml for 24 h had no significant effect on basal glucose uptake, insulin sensitivity or maximal insulin responsiveness. C(I-150) values (means+/-S.E.M.) were as follows: basal, 91.2+/-13 nM; 1 ng/ml TNF-alpha, 102+/-12 nM; and basal, 70.8+/-13 nM; 10 ng/ml TNF-alpha, 43.7+/-40 nM. PKC inhibition markedly attenuated glucose uptake, but there was no difference in insulin sensitivity with RO-318220 alone compared with RO-318220+TNF-alpha. In conclusion, although increased TNF-alpha expression and plasma concentrations have been implicated in the pathogenesis of insulin resistance in various clinical states, there is no evidence that TNF-alpha impairs insulin-stimulated glucose uptake in a skeletal-muscle-derived cell line.
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PMID:Effects of tumour necrosis factor-alpha and inhibition of protein kinase C on glucose uptake in L6 myoblasts. 1099 95

Streptococcus agalactiae (group B streptococcus, GBS) is the major pathogen of neonatal sepsis. In some newborns, GBS sepsis may have a severe course, including septic shock with a high mortality rate, whereas other newborns are colonized with GBS on their surfaces without any clinical signs of bacterial infection. The reason for this discrepancy is far from clear. We sought, in this study, to compare cytokine expression in cord blood mononuclear cells after stimulation with GBS strains isolated from newborns with sepsis, and strains isolated from newborns without any symptoms of invasive infection. Cord blood mononuclear cells were incubated with either heat-killed bacteria of different strains or lipopolysaccharide, respectively. After 6 and 24 h, cells were harvested and cytokine mRNA-expression was analyzed by reverse-transcriptase PCR. Likewise, supernatants were tested for IL-6 and tumor necrosis factor-alpha concentrations by enzyme immunoassay. When comparing IL-6 and tumor necrosis factor-alpha secretion, there were significantly higher IL-6 levels after stimulation with sepsis than with colonizing isolates. Likewise, mRNA expression of IL-6, IL-1 beta, and IL-12p40 was significantly higher after stimulation with sepsis isolates. This was also true when normalizing to cytokine expression after stimulation with lipopolysaccharide. These findings indicate that the different clinical pictures in response to GBS, either septic infection or colonization, might reflect strain-specific properties. If the respective characteristics can be defined, it might become possible to distinguish by molecular methods potentially "dangerous" from "harmless" strains. Moreover, our findings underline the essential role of these cytokines in the pathogenesis of neonatal GBS sepsis.
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PMID:Different cytokine expression in cord blood mononuclear cells after stimulation with neonatal sepsis or colonizing strains of Streptococcus agalactiae. 1132 54

A novel fimbrial type in Escherichia coli was identified and characterized. The expression of the fimbria was associated with the O18acK1H7 clonal group of E. coli, which cause newborn meningitis and septicemia when grown at low temperature; hence, it was named the Mat (meningitis associated and temperature regulated) fimbria. The fimbriae were purified from a fimA::cat sfaA::Gm fliC::St derivative of the O18K1H7 isolate E. coli IHE 3034. The purified Mat fimbrillin had an apparent molecular mass of 18 kDa and did not serologically cross-react with the type 1 or S fimbria of the same strain. The matB gene encoding the major fimbrillin was cloned from the genomic DNA of the fimA::cat sfaA::Gm fliC::St derivative of IHE 3034. The predicted MatB sequence was of 195 amino acids, contained a signal sequence of 22 residues, and did not show significant homology to any of the previously characterized fimbrial proteins. The DNA sequence of matB was 97.8% identical to a region from nucleotides 17882 to 18469 in the 6- to 8-min region of the E. coli K-12 chromosome, reported to encode a hypothetical protein. The 7-kb DNA fragment containing matB of IHE 3034 was found by restriction mapping and partial DNA sequencing to be highly similar to the corresponding region in the K-12 chromosome. Trans complementation of the matB::cat mutation in the IHE 3034 chromosome showed that matB in combination with matA or matC restored surface expression of the Mat fimbria. A total of 27 isolates representing K-12 strains and the major pathogroups of E. coli were analyzed for the presence of a matB homolog as well as for expression of the Mat fimbria. A conserved matB homolog was found in 25 isolates; however, expression of the Mat fimbriae was detected only in the O18acK1H7 isolates. Expression of the Mat fimbria was temperature regulated, with no or a very small amount of fimbriae or intracellular MatB fimbrillin being detected in cells cultivated at 37(o)C. Reverse transcriptase PCR and complementation assays with mat genes controlled by the inducible trc promoter indicated that regulation of Mat fimbria expression involved both transcriptional and posttranscriptional events.
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PMID:matB, a common fimbrillin gene of Escherichia coli, expressed in a genetically conserved, virulent clonal group. 1146 75

Patients with chronic hepatitis C frequently report tiredness, easy fatigability, and depression. The aim of this study is to determine whether hepatitis C virus (HCV) replication could be found in brain tissue in patients with hepatitis C and depression. We report two patients with recurrent hepatitis C after liver transplantation who also developed severe depression. One patient died of multiorgan failure and the other, septicemia caused by Staphylococcus aureussis. Both patients had evidence of severe hepatitis C recurrence with features of cholestatic fibrosing hepatitis. We were able to study samples of their central nervous system obtained at autopsy for evidence of HCV replication. The presence of HCV RNA-negative strand, which is the viral replicative form, was determined by strand-specific Tth-based reverse-transcriptase polymerase chain reaction. Viral sequences were compared by means of single-strand conformation polymorphism and direct sequencing. HCV RNA-negative strands were found in subcortical white matter from one patient and cerebral cortex from the other patient. HCV RNA-negative strands amplified from brain tissue differed by several nucleotide substitutions from serum consensus sequences in the 5' untranslated region. These findings support the concept of HCV neuroinvasion, and we speculate that it may provide a biological substrate to neuropsychiatric disorders observed in patients with chronic hepatitis C. The exact lineage of cells permissive for HCV replication and the possible interaction between viral replication and cerebral function that may lead to depression remain to be elucidated.
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PMID:Detection of hepatitis C virus sequences in brain tissue obtained in recurrent hepatitis C after liver transplantation. 1242 14


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