Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A variety of cytokines secreted by cells of the immune system could contribute to the induction or persistence of the inflammatory processes in autoimmune and infectious diseases. Soluble CD23 (sCD23) and interleukin-4 (IL-4) are the recently characterized factors implicated in B cell-T cell function in human disease. In this study we examined the circulating levels of sCD23, IL-4, and soluble interleukin-2 receptors (sIL-2R) from patients with hepatitis B surface antigen-positive (HBsAg+) acute viral hepatitis (AVH), HBsAg+ chronic active hepatitis (HBsAg+ CAH), and autoimmune chronic active hepatitis (AICAH) and from autoimmune rheumatic disease patients, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). The sCD23 was found in sera from 16 of 16 patients with AICAH (159.0 +/- 40.8 ng/ml), in 3 of 32 patients with AVH (4.1 +/- 15.6), 5 of 30 patients with HBsAg+ CAH (6.9 +/- 17), 8 of 25 patients with SLE (19.4 +/- 37.2), 2 of 21 patients with RA (4.7 +/- 16.3), and none of the 50 age-matched healthy controls. However, sIL-2R was detected more frequently in sera from all hepatitis and rheumatic disease patients. In AICAH, sCD23 levels correlated positively with IL-4 (r = 0.44, P = 0.001) but not with sIL-2R. Markedly elevated levels of sCD23 and IL-4 in serum are prominent and characteristic features of AICAH disease, which could play an important role in the pathogenesis or induction and perpetuation of the inflammatory response in this disorder.
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PMID:Soluble CD23 and interleukin-4 levels in autoimmune chronic active hepatitis and systemic lupus erythematosus. 813 57

To investigate the state of activation of T lymphocytes in hemodialysis patients with chronic hepatitis C, serum levels of soluble interleukin-2 receptors (sIL-2R), interleukin-2 (IL-2) and expression of interleukin-2 receptors (IL-2R) on peripheral T lymphocytes were measured in 30 hemodialysis patients with chronic hepatitis C, 14 hemodialysis patients without hepatitis, 30 patients with chronic hepatitis C and 41 normal subjects. A significant increase in sIL-2R levels was noted in all patients with chronic hepatitis compared to normal controls. This increase was even more significant in hemodialysis patients, while a less significant increase was also found in hemodialysis patients without hepatitis C viral infection. Expression of IL-2R on T lymphocytes was increased only in hemodialysis patients with chronic hepatitis. All patients had low levels of serum IL-2. These findings show that a T-cell activation involving the IL-2 system is present in chronic hepatitis C and that this activation is more prominent in hemodialysis patients, probably due to additional extrahepatic factors.
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PMID:Interleukin 2-dependent immunoregulatory function in hemodialysis patients with chronic hepatitis C. 857 31

A single intravenous injection of concanavalin A (Con A) induces T-cell activation and an acute hepatitis in mice. This study investigated the role of interferon gamma (IFN-gamma) in the pathogenesis of this hepatitis model. Striking increases in the plasma levels of various cytokines, including tumor necrosis factor (TNF), interleukin-2 (IL-2), and IFN-gamma, were detected before the increase in plasma aminotransferase levels induced by Con A injection. TNF levels peaked within 2 hours, whereas IFN-gamma levels peaked at 6 hours after Con A injection. In contrast to a sharp peak of TNF levels, high IFN-gamma levels were detected for a more prolonged period. Passive immunization with anti-IFN-gamma monoclonal antibody (MAb) conferred a dose-dependent protection against liver injury in this model. This protection was observed when anti-IFN-gamma MAb was administered at least 30 minutes before Con A injection but not when given 1 hour after Con A injection. The protection from Con A-induced hepatitis was also induced by administration of rIL-6 before Con A injection. rIL-6 treatment induced significant albeit incomplete inhibition of IFN-gamma and TNF production, whereas this regimen did not affect IL-2 production. Despite striking protective effects of rIL-6 or anti-IFN-gamma MAb, comparable levels of cellular (both T cell and polymorphonuclear cell) infiltration were detected in liver sections from animals untreated, or treated with either rIL-6 or anti-IFN-gamma MAb. Moreover, electron microscopic examination showed that infiltrating T cells exhibited a blastoid appearance in all groups. These results indicate that IFN-gamma plays a critical role in the development of Con A-induced acute hepatitis and suggest that IL-6 administration can regulate the manifestation of hepatitis through mechanisms including the reduced production of inflammatory cytokines such as IFN-gamma.
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PMID:Critical involvement of interferon gamma in the pathogenesis of T-cell activation-associated hepatitis and regulatory mechanisms of interleukin-6 for the manifestations of hepatitis. 867 84

Clinical studies with the human anti-idiotypic antibody 105AD7 have clearly shown that 791Tgp72 is a good target antigen for cell-mediated immunity. No antibody-related toxicity was observed in any of the 135 patients entered into phase I/II clinical trials of 105AD7, whereas both helper and cytotoxic T-cell responses were induced. The helper responses were exemplified by induction of interleukin-2 (IL-2), antigen-specific blastogenesis, and enhanced natural killer (NK) activity. Anti-tumor cytotoxicity was measured directly and was supported by activation of circulating CD8 cells. In this study, it is shown that a 100-microgram injection of 105AD7 was more effective than the 200-microgram dose. Enhanced IL-2 production was observed following 15/19 injections of 100 micrograms of 105AD7 whereas only 4/11 injections of 200 micrograms of 105AD7 induced responses (p < 0.02). Similarly, time to progression was significantly (p < 0.05) slower (median 6 m) in patients injected with 100 micrograms than patients receiving the higher dose, suggesting that 100 micrograms or lower may be the optimal dose. The standard dose for hepatitis vaccination is 10 micrograms. In vitro blastogenesis assays on naive donors have shown that a dose of 105AD7, which is either too high or too low, fails to activate T cells. The optimal dose in vitro is 10 ng.
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PMID:Low doses of 105AD7 cancer vaccine preferentially stimulate anti-tumor T-cell immunity. 908 24

Although numerous studies on abnormality of neutrophil function in patients with viral hepatitis have previously been reported, little is known about mechanisms of neutrophil dysfunction. To investigate mechanisms of neutrophil dysfunction in these patients, neutrophil membrane fluidity was measured by fluorescence polarization technique in 76 hepatitis patients. The results showed that membrane fluidity of neutrophils from patients with chronic active hepatitis (CAH) or subfulminant hepatic failure (SFHF) was much lower than that in normal controls (p < 0.01), but such a difference could not be found in patients with acute hepatitis (p > 0.05). Furthermore, recombinant interleukin-2 could significantly increase membrane fluidity, while lipopolysaccharide decreased membrane fluidity of neutrophils (p < 0.01, p < 0.001). The present study indicates that there is abnormal membrane fluidity of neutrophils in patients with CAH and SFHF. Neutrophil dysfunction in hepatitis patients may be partly due to altered membrane fluidity.
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PMID:The determination of neutrophil membrane fluidity in patients with hepatitis B: a fluorescence polarization study. 916 74

The liver injury in the concanavalin A (Con A)-induced mouse hepatitis model has been well studied. However, there has been little study on the effects of Con A on extrahepatic organs. The aim of the present work was to determine the effects of Con A on the spleen, kidney and lung. A histopathological study showed that Con A (15 mg/kg, i.v.) administration affects not only the liver, but also all these extrahepatic organs. Messenger RNA expression was studied by the using polymerase chain reaction. Treatment with Con A induced interleukin-2 mRNA in the spleen, but only slightly induced it in the kidney. The mRNAs of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) were induced in all these organs. At 24 hr after Con A treatment, the expression of IFN-gamma mRNA, but not that of TNF-alpha mRNA, was inhibited by cyclosporine A (50 mg/kg, i.p.), suggesting that Con A induced these cytokine mRNAs through different mechanisms. In the kidney and lung, CD4+ and CD8+ T-cell infiltration was suggested by the Con A-induced CD4 and CD8 mRNAs. The present study showed the histopathological effects of Con A and Con A-induced cytokine mRNA expression on the spleen, kidney and lung.
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PMID:Expression of cytokine mRNA in extrahepatic organs in a mouse concanavalin A-hepatitis model. 971 69

Treatment of mice with concanavalin A (Con A) induced interleukin-2 (IL-2) mRNA expression in the liver, which might be a result of Con A-induced T-cell activation. Pretreatment with cyclosporine A (CsA) (50 mg/kg, i.p.) or dexamethasone (DEX) (2.5 mg/kg, i.p.) inhibited the Con A-induced liver injury, as assessed by the plasma alanine aminotransferase level, by 85% and 95%, respectively. CsA inhibited the Con A-induced IL-2 mRNA expression completely, whereas DEX only partially inhibited it. Thus CsA seems to prevent Con A-induced hepatitis mainly by inhibiting T-cell activation. In the case of DEX, rather than by inhibiting Con A-induced T-cell activation, it may prevent Con A-induced hepatitis through other means.
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PMID:Effects of immunosuppressants on concanavalin A-induced interleukin-2 mRNA expression in mouse liver. 971 75

The administration of concanavalin A (Con A) to mice induces cytokine-dependent hepatitis. In the present study, the effect of glycyrrhizin on Con A-induced hepatitis was examined. Treatment of mice with Con A (0.2 mg/mouse, i.v.) induced elevation of the plasma transaminase activities at 24 h. Mice were treated with glycyrrhizin (100, 200 and 400 mg/kg, i.p.), and glycyrrhizin at the doses of 200 and 400 mg/kg inhibited the Con A-induced elevation of the plasma transaminase activities. At 1 h after Con A treatment, interferon-gamma, tumor necrosis factor-alpha, interleukin-2 and interleukin-6 proteins were released into the plasma. Although treatment with glycyrrhizin at 200 mg/kg inhibited Con A-induced hepatitis, it did not affect the release of any of these Con A-induced cytokines into the plasma. The present results clearly show that glycyrrhizin inhibited Con A-induced hepatitis without affecting cytokine expression.
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PMID:Glycyrrhizin protects mice from concanavalin A-induced hepatitis without affecting cytokine expression. 1040 81

Hepatitis C virus (HCV) is responsible for most cases of posttransfusion hepatitis and sporadic or community-acquired non-A, non-B hepatitis. Different generations of enzyme-linked immunosorbent assay have been generated for detecting antibodies to HCV epitopes. HCV-RNA quantitative analysis has been developed by means of polymerase chain reaction technique. This approach is the only reliable method for HCV-RNA tissue localization, being helpful in early diagnosis. HCV infected liver is characterized by an inflammatory infiltrate including CD4+, CD8+, and B lymphocytes. Evidence has been provided that in HCV patients CD8+ cell response is associated with low level of viraemia and higher level of disease activity. CD4+ T cells exhibit specificity for the core antigen, also correlating with disease activity and viraemia. Costimulatory molecules, cytokines, oxygen radicals, the complex Fas/Fas-ligand and soluble class I HLA structures are discussed as putative cofactors involved in disease evolution. Various forms of interferon (IFN)-alpha have been evaluated for the treatment of patients with HCV infection. Initial enthusiasm has been attenuated by the evidence of a low sustained virological response rate and the constant side effects of IFN-alpha therapy in patients with chronic HCV disease. Among possible markers for predicting therapeutic outcome in HCV-positive individuals, anti-core antibodies correlate positively with response to IFN-alpha administration, as well as reduction of interleukin-2 serum levels has been detected in patients with a good therapeutic response. Association between HCV infection and autoimmune phenomena, also in relation to IFN-alpha therapy has been reported. Finally, results of the combined treatment with IFN-alpha/ribavirin are illustrated.
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PMID:Hepatitis C virus infection: immune responsiveness and interferon-alpha treatment. 1063 75

To assess the relationship between serum cytokine behavior and treatment outcome in type 1 autoimmune hepatitis, serum levels of interferon-gamma, interleukin-2, interleukin-4, and interleukin-10 were measured by enzyme immunoassay in 43 patients and 20 normal subjects. Serum samples were similarly tested in 38 patients after corticosteroid treatment. Serum levels of interleukin-2 and interleukin-4 were significantly lower in patients than in normal subjects. Interleukin-2 was the least common cytokine detected before (3%), during (0%), or after treatment (0%). Serum levels of interleukin-10 at presentation did not differ from those of normal subjects but they did decrease during therapy, especially in patients who entered remission. Changes in these levels, however, did not always parallel treatment outcome or histological activity. We conclude that serum levels of interleukin-2 and interleukin-4 are lower than normal in type 1 autoimmune hepatitis. Serum concentrations of interleukin-10 diminish during corticosteroid therapy but changes do not closely reflect outcome. The rarity of interleukin-2 in serum may be a distinguishing feature.
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PMID:Nature and behavior of serum cytokines in type 1 autoimmune hepatitis. 1079 72


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