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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Natural infection by mouse hepatitis virus (MHV) can affect interpretation of immunological studies in mice. MHV, a collective term describing a group of corona viruses, is found in natural infections in over 70% of laboratory mouse populations in the U.S.A. and Canada. Natural outbreaks of MHV in our animal colony afforded us the opportunity to study MHV-induced immunosuppression as well as the effects of MHV infection on neurotransmitter immunomodulation. Concanavalin A (Con A)-stimulated DNA synthesis by spleen T lymphocytes from MHV-infected mice was 20-50% that of non-infected mice. The MHV infection also altered neurotransmitter modulation of spleen T-lymphocyte activation. In contrast to noradrenaline ablation of Con A-activated DNA synthesis by spleen lymphocytes from non-infected mice, DNA synthesis by the infected group was not inhibited by noradrenaline or dibutyryl-cAMP. These effects of MHV infection were specific for spleen T lymphocytes since MHV infection did not alter Con A stimulation of thymocytes, lipopolysaccharide stimulation of spleen B lymphocytes, or noradrenaline inhibition of thymocyte and B-cell DNA synthesis. MHV infection also did not alter spleen T-lymphocyte subset proportions. Thus, MHV infection inhibits spleen T-lymphocyte activation and blocks in vitro catecholamine and cAMP regulation of spleen T-cell activation but does not affect activation of thymic cells or spleen B cells.
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PMID:Mouse hepatitis virus infection suppresses modulation of mouse spleen T-cell activation. 157

Plasma of cAMP and cGMP in 30 cases of chronic active hepatitis (group of cholestatic patients) as well as in 20 cases of chronic hepatitis with submassive or massive necrosis (group of chronic severe hepatitis patients) were studied with 125I-marked radioimmunoassay. 50 cases with their serum bilirubin levels higher than 171 mumol/L were selected as subjects for this study. Among them, 42 were diagnosed as hepatitis B, 6 as coinfection of hepatitis A and B. According to differentiation of symptoms and signs of TCM, 24 were diagnosed as simple hepatitis due to blood stasis and blood heat, 17 as hepatitis due to blood stasis and blood heat accompanying symptoms of Yang deficiency of the Spleen and Kidney. 20 healthy persons were selected as controls. The results were as follows: cAMP was 56.82 +/- 25.54 ng/L and 80.32 +/- 20.73 ng/L, and cGMP was 9.07 +/- 6.56 ng/L and 19.49 +/- 9.34 ng/L in the group of cholestatic patients and in the group of chronic severe hepatitis patients respectively. Both were higher than those in the control group whose cAMP was 14.12 +/- 3.25 ng/L and cGMP was 5.87 +/- 1.44 ng/L (P less than 0.01). Increase in cGMP and decrease in the ratio of cAMP and cGMP in the cases accompanying symptoms of Yang deficiency of the Spleen and Kidney were much higher than those in the other two types of hepatitis patients (P less than 0.01 and 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relation of changes in plasma cAMP, cGMP and the clinical conditions, pathology and the type of traditional Chinese medicine in 50 cases of chronic severe icteric hepatitis]. 216 73

Among the large spectrum of pharmacological activities of flavonoids, play an important role the recently investigated properties involving the arachidonic acid metabolism. In order to clarify the mechanisms of "cytoprotection" of the 3-palmitoyl-(+)-catechin (Palm-cat), a new flavonoid compound (C31 H44 O7) we have studied in experimental hepatitis of the rat, induced by Galactosamine (Ga1N) and E. coli 055:B 5 endotoxin (LPS), hepatic cAMP and cGMP, transaminases, bilirubin and endotoxemia. The Palm-cat significantly increases cyclic-GMP levels in the liver, whereas reduces or slightly modifies the cAMP. Transaminases and bilirubin values increase both in controls and flavonoid treated rats. The flavonoid significantly decreases the frequency of endotoxemia. These effects suggest that RES and hepatocytes functions, immune and inflammatory response can be affected in liver disease by flavonoids via cyclic nucleotides regulation.
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PMID:Flavonoids and hepatic cyclic monophosphates in liver injury. 608 50

The induction of macrophage procoagulant activity (PCA) has been shown to correlate with the development of fulminant hepatic necrosis after infection with murine hepatitis virus strain 3 (MHV-3). However, comparatively little is known about the early events in cells after viral infection leading to PCA expression. Accordingly, we investigated the early cellular events in the induction of macrophage PCA by MHV-3. MHV-3 stimulation of macrophages did not result in a detectable increase in intracellular calcium levels nor did stimulation of macrophages by calcium ionophores result in induction of PCA, suggesting that calcium transients were neither necessary nor sufficient for induction of PCA by MHV-3. Treatment of cells with phorbol myristate acetate had no effect on PCA induction; however, inhibition of protein kinase C (PKC) by staurosporine or H7 resulted in attenuation of macrophage PCA following MHV-3 stimulation (P < 0.05 compared with untreated macrophages), suggesting that although activation of PKC alone is insufficient for PCA induction, PKC may be an integral component of PCA induction by MHV-3. We have previously demonstrated that dimethyl prostaglandin E2 inhibited induction of PCA by MHV-3. In this study, treatment of cells by agents that increase intracellular cAMP (forskolin, isobutylmethyl xanthine) significantly inhibited PCA induction (P < 0.02). These results demonstrate that induction of macrophage PCA by MHV-3 involves PKC, but proceeds independently of changes in intracellular calcium, and that PCA expression is down-regulated by increases in intracellular cAMP.
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PMID:Effect of alterations in early signal transduction events on the induction of procoagulant activity by murine hepatitis virus strain 3 in vitro. 773 Aug 2

Impairments of the cAMP system in rat liver tissue are of importance in pathogenesis of acute heliotrin hepatitis. Such drugs as phosphatidylcholine, ecdystene, unithiol promote the impaired lipid environment restoration which makes it possible to normalize the adenylate cyclase system and cyclic nucleotides functions.
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PMID:[Changes in the adenylate cyclase system of rat liver cells in acute experimental hepatitis and ways of correcting them]. 797 77

Knowledge continues to grow on the biology of endogenous erythropoietin (EPO), its effects on red blood cell physiology, and the use of the recombinant form of the hormone. In addition to oxygen delivery, oxygen consumption may be important in stimulating EPO production. This production is likely mediated by an intracellular messenger system other than cAMP. Once released, EPO prevents programmed cell death of BFU-E and CFU-E cells. Recent evidence suggests that lack of EPO, rather than the presence of EPO inhibitors, is the cause of the anemia seen in renal patients. Recombinant EPO has been available clinically since mid 1989. Nearly two thirds of dialysis patients are receiving this agent, although low doses are the rule, with the average hematocrit achieved of only 31%. EPO dosing has been subjected to kinetic modeling that has revealed a wide range in RBC half-life from patient to patient. This accounts in part for the varying maintenance dosing requirements. An additional modulating factor in the response to EPO is severe, secondary hyperparathyroidism with bone marrow fibrosis which may be reversible with medical or surgical parathyroidectomy. Hypertension continues to occur in 20-35% of patients given EPO. This effect may be mediated by endothelin which appears to be stimulated by EPO administration. Treatment of the anemia of renal failure leads to many organ system benefits including improved muscle metabolism, decreased left ventricular hypertrophy, enhanced immune responses to hepatitis vaccine, and improved brain electrophysiology. he optimal target hematocrit to achieve the greatest benefits for the patient at an acceptable cost remains to be determined.
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PMID:Erythropoietin overview--1993. 798 77

Pg E, F2 alpha and F1 alpha, protein-bound plasmic oxyproline (PBPO) as well as 24-h oxyprolinuria (OPU) were measured in 119 patients suffering from various forms of chronic hepatic diseases. Composition of cellular infiltrates in histological specimens was assessed quantitatively for chronic hepatitis patients. Hepatic levels of Pg E, OPU and PBPO were elevated in all the patients, whereas PgF2 alpha and 6-keto-PgF1 alpha values were similar to controls. There were relationships between PBPO and OPU, PgE and 6-keto-PgF1 alpha. Unlike patients with active hepatitis and hepatic cirrhosis, those with chronic persistent hepatitis demonstrated a direct correlation between cellular infiltrate fibroblasts and PgE, PgF2 alpha; between PgF2 alpha and Kupffer's cells content. Inverse relationship occurred between PgE and free hepatic macrophages. In response to prostenon (PGE2) moderate PBPO decline went in line with elevation of cAMP/cGMP. A significant increase of PBPO during introduction of ensaprost-F (PgF2 alpha) did not result in changes in cyclic nucleotides. Prostenon treatment decreased PBPO under no shifts in OPU. A regulatory role of PgE is suggested in collagen metabolism stabilization. Prostenon is proposed for therapeutic use to inhibit sclerotic processes in liver impairment.
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PMID:[Prostaglandins and collagen metabolism in chronic liver diseases]. 801 21

The X gene product of the human hepatitis B virus (HBx), a major factor responsible for hepatitis and hepatocellular carcinoma, modulates transactivation by a variety of transcription factors. Herein, expression of the phosphoenolpyruvate carboxykinase (PEPCK) gene was found to be regulated transcriptionally by HBx through two distinct promoter regions. The cAMP response element (CRE)-1 site within the proximal promoter region mediated the HBx-induced transactivation of the PEPCK gene through C/EBP alpha and ATF-2. A retinoid X receptor (RXR) response element within the distal promoter region also contributed to the HBx-induced transactivation. Consistent with these results, HBx directly interacted with RXR, and the interaction interfaces were localized to the transactivation domain of HBx and the ligand binding domain of RXR.
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PMID:Direct binding of hepatitis B virus X protein and retinoid X receptor contributes to phosphoenolpyruvate carboxykinase gene transactivation. 1104 64

Hepatoma cell lines can produce a massive amount of chemokines in response to various stimuli including hepatitis viruses and their products. However, it remains elusive on the types of chemokine receptor(s) expressed in the hepatoma tissues and its roles in hepatoma development. To clarify these points, we examined the chemokine receptor expression in six human hepatoma cell lines. All of the hepatoma cell lines constitutively and exclusively expressed CCR1 mRNA and its protein on their cell surface. CCR1 expression was also detected on hepatoma cells and to a lesser degree, on endothelial cells in hepatoma tissues but not in normal liver tissues. Furthermore, CCL3 expression was detected in hepatoma cells, endothelial cells, and to a lesser degree, fibroblast-like cells in hepatoma tissue, whereas only occasional vascular endothelial cells and inflammatory cells in normal liver tissues were weakly positive for CCL3. Moreover, the forskolin-mediated increases in intracellular cAMP concentrations were inhibited by the ligands for CCR1, CCL3, CCL4, and CCL5, suggesting that the expressed CCR1 was functional. Four hepatoma cell lines produced CCL3 only in response to interleukin (IL)-1 alpha and IL-1 beta. Finally, IL-1 alpha and IL-1 beta were detected abundantly in hepatoma tissues but not in normal liver tissues. Thus, IL-1 may enhance the local production of CCL3, which may interact with CCR1 expressed on hepatoma cells, in an autocrine and/or paracrine manner.
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PMID:Potential interaction between CCR1 and its ligand, CCL3, induced by endogenously produced interleukin-1 in human hepatomas. 1265 17

Vasoactive intestinal peptide (VIP) is well characterized as an endogenous anti-inflammatory neuropeptide and has a brand range of biological functions. In this study, we found increased endogenous VIP expression in mice with concanavalin A-induced hepatitis, a widely used experimental model of immune-mediated liver injury. We investigated further the effect of VIP administration on concanavalin A-induced liver injury. Compared with mice pretreated with PBS, mice pretreated with VIP exhibited much lower plasma levels of aminotransferases, less inflammatory infiltration in the liver and hepatocyte apoptosis. Meanwhile, VIP significantly inhibited the release of inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in concanavalin A-injected mice, but markedly elevated the production of anti-inflammatory cytokine interleukine-10 (IL-10). Further investigation demonstrated increased intracellular cAMP concentration after VIP administration, and showed that the protective effect of VIP on concanavalin A-induced hepatitis was mediated mainly through VIP receptor 1 (VPAC(1)). These results suggest that VIP is capable of attenuating immune-mediated liver injury in vivo. This effect is associated with its downregulation of critical inflammatory mediators and its upregulation of anti-inflammatory cytokine through VPAC(1), possibly via the cAMP-dependent pathway.
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PMID:Vasoactive intestinal peptide attenuates concanavalin A-mediated liver injury. 1922 97


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