Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant pleural or peritoneal effusion-associated lymphoid (EAL) cells from 17 patients with advanced carcinoma were cultured with autologous carcinoma cells in the presence of either recombinant interleukin 2 (rIL 2) or T-cell growth factor (TCGF). Considerable cytolytic activity of the cells against allogeneic tumor cells, such as K562 and Daudi cells was induced by the cultivation. TCGF-activated EAL cells acquired higher anti-Daudi tumor cytotoxicity than rIL 2-activated EAL cells. The resultant TCGF-activated EAL cells from cancer patients significantly exceeded lytic activity of TCGF-activated EAL cells from patients with liver cirrhosis for control (p less than 0.01). Four of 6 cases examined also showed cytotoxic activity against autologous tumor. In facts, viable carcinoma cells co-cultured with EAL cells and TCGF mostly disappeared during 14 days. Similar phenomenon was not observed in rIL 2-activated EAL cells. Thus, it was suggested that more additional lymphokine other than IL 2 was necessary to generate cytotoxic activity against autologous tumor cells. The cell populations responsible for cytolytic activity to allogeneic and/or autologous tumor cells were investigated by two-color flow cytometry. The majority of killer-effector cells against allogeneic cells in rIL 2-activated EAL cells from cancer patients showed CD4+Leu8- phenotype at population level. In contrast, it was suggested that cytolytic activity against allogeneic and/or autologous tumor cells in TCGF-activated EAL cells might be mediated by CD8+ CD11- and CD8+ CD28+ effector cells.
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PMID:Functional and phenotypic characteristics of effusion-associated lymphoid cells cultured in the presence of either recombinant interleukin 2 or T-cell growth factor from malignant pleural and peritoneal effusions in patients with advanced carcinoma. 207 78

We investigated the production of tumor necrosis factor alpha by peripheral blood mononuclear cells of patients with chronic liver disease and its association with hepatitis activity. Tumor necrosis factor alpha production was measured with an enzyme-linked immunosorbent assay. Tumor necrosis factor alpha production by peripheral blood mononuclear cells stimulated with recombinant gamma-interferon of patients with chronic active hepatitis (5.8 +/- 4.0 units per ml, p less than 0.05) and patients with cirrhosis (4.1 +/- 2.1 units per ml, p less than 0.05) was significantly increased when compared with controls (2.5 +/- 1.6 units per ml). Tumor necrosis factor alpha production by peripheral blood mononuclear cells stimulated with a combination of recombinant gamma-interferon and recombinant interleukin 2 of patients with chronic persistent hepatitis (5.8 +/- 3.8 units per ml, p less than 0.05), patients with chronic active hepatitis (8.9 +/- 3.0 units per ml, p less than 0.001) and patients with cirrhosis (6.7 +/- 3.2 units per ml, p less than 0.05) was significantly increased in comparison with controls (3.3 +/- 1.8 units per ml). Tumor necrosis factor alpha production of patients with chronic active hepatitis was significantly higher than that of patients with chronic persistent hepatitis (p less than 0.05). There was a significant correlation (r = 0.5699, p less than 0.005) between tumor necrosis factor alpha production and histologic activity index in patients with chronic persistent hepatitis or chronic active hepatitis. These findings show that tumor necrosis factor alpha production is increased in chronic liver disease and that the increased tumor necrosis factor alpha production is related to hepatitis activity.
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PMID:Tumor necrosis factor alpha production by peripheral blood mononuclear cells of patients with chronic liver disease. 255 75

The present study was undertaken to examine early T lymphocyte activation in chronic hepatitis B virus (HBV) carriers. Nineteen hepatitis B surface antigen-positive patients (eight with liver cirrhosis and 11 with chronic hepatitis) and 18 healthy controls were studied in a period free of other infection. Mitogen-stimulated cellular interleukin 2 receptor expression, soluble interleukin 2 receptor release, and interleukin 2 production were studied in peripheral blood mononuclear cells cultured for 24 h. No difference was demonstrated between the patients and healthy controls in the cellular interleukin 2 receptor expression, soluble interleukin 2 receptor release, and interleukin 2 production. Pokeweed mitogen-stimulated interleukin 2 production in lymphocytes from cirrhotic patients was significantly lower than that of the noncirrhotic patients. However, the cellular and soluble interleukin 2 receptor levels did not differ between the two groups of chronic HBV carriers. Despite the fact that it has been suggested that autoreactive T cells have a role in mediating the development of chronic liver diseases associated with HBV infection, this study fails to demonstrate a defective T lymphocyte activation in these patients. The observed reduction of interleukin 2 production from activated lymphocytes may be related to the severity of liver impairment, rather than the HBV infection itself.
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PMID:T lymphocyte activation in chronic hepatitis B infection: interleukin 2 release and its receptor expression. 259 55

Interferon-gamma (IFN-gamma) was induced from a human peripheral mononuclear fraction by incubation with a streptococcal preparation stabilized with penicillin G (OK432). This IFN-gamma-producing activity was significantly reduced in patients with chronic hepatitis and hepatocellular carcinoma. In patients with liver cirrhosis it was also reduced but not significantly. Serum hepatitis B virus DNA and skin tests for the purified protein derivative of tuberculin, phytohemagglutinin-P and a polysaccharide fraction prepared from streptococcus pyogenes Su strain were determined to have no significant relation to this IFN-gamma-producing activity. Although the addition of interleukin 2 (IL-2) to the culture medium enhanced the IFN-gamma-producing activity, there was no difference in this enhancement between normal control and chronic hepatitis. Therefore reduction of the IFN-gamma-producing activity observed in chronic hepatitis seems to be caused by a decreased number of IFN-gamma-producing activity cells or hypofunction of these cells or both. Since HBeAg became negative in patients whose IFN-gamma-producing activity was increased by the administration of the immunopotentiator OK432 or IFN-beta, the IFN-producing system in the patients with B type hepatitis may contribute to the elimination of HBV. Adenine arabinoside suppressed IFN-gamma-producing activity both in vivo and in vitro.
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PMID:In vitro interferon producing activity of peripheral mononuclear cells in patients with chronic liver disease. 303 38

Soluble interleukin 2 receptors (sIL 2R) in the sera of patients with viral liver diseases were quantified with a solid-phase enzyme immunoassay using two monoclonal antibodies against the receptors. The sIL 2R levels in patients with acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma were significantly higher than those in control subjects. In acute hepatitis patients, the high levels of sIL 2R observed during the florid stage returned to normal during remission. Levels in patients with chronic active hepatitis were significantly higher than in those with chronic persistent and lobular hepatitis, and levels observed during the exacerbation phase of chronic hepatitis were higher than they were during remission. Thus, in chronic hepatitis, sIL 2R levels increased in proportion to the inflammatory activity, and correlated well with serum transaminase (glutamic oxaloacetic transaminase: SGOT, glutamic pyruvic transaminase: SGPT) activities, but not with blood urea nitrogen or creatinine concentrations. In patients with a high degree of focal and piecemeal necrosis, serum sIL 2R levels increased further during recombinant interleukin 2 therapy. In post-hepatitic liver cirrhosis and hepatocellular carcinoma, sIL 2R levels correlated with serum cholinesterase and creatinine concentrations, but not with transaminase activities. Measurement of serum sIL 2R levels in patients with liver disease but without renal injury, may help in the diagnosis of inflammation in hepatitis, a process in which interleukin 2 may participate.
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PMID:Increased serum soluble interleukin 2 receptor levels in patients with viral liver diseases. 306 11

We investigated the role of the interferon system in the pathogenesis of chronic liver disease. Interferon-gamma production by peripheral blood mononuclear cells was measured with an ELISA. While concanavalin A-stimulated and recombinant interleukin 2-stimulated production of interferon-gamma in patients with chronic active hepatitis and liver cirrhosis was significantly decreased when compared with that of controls (518 +/- 189 and 729 +/- 195 units per ml, mean +/- S.D.), there was also a lot of overlap. Addition of indomethacin to the cultures partially restored interferon-gamma production in patients with chronic active hepatitis and liver cirrhosis, indicating that suppressor function of monocytes was, in part, responsible for the diminished interferon-gamma production. Serial studies showed that interferon-gamma production rose during acute deterioration of illness, during treatment with interleukin 2 and with the improvement of clinical course. Interferon-gamma production was not different among hepatitis B e antigen or antibody positive, and non-A, non-B patients with chronic active hepatitis and liver cirrhosis. Our findings suggest that diminished interferon-gamma production is associated with disease severity in chronic liver disease, irrespective of the hepatitis B virus carrier state. It would be interesting to compare the efficacy of treatment with interferon-gamma or interferon-gamma inducers such as interleukin 2 in chronic hepatitis B patients with and without decreased in vitro interferon-gamma production.
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PMID:Interferon-gamma production by peripheral blood mononuclear cells of patients with chronic liver disease. 310 84

Proliferation and IgG synthesis of peripheral blood mononuclear cells (PBMC) in response to stimulation with recombinant interleukin 2 (IL-2) and Staphylococcus aureus Cowan 1 (SAC) were evaluated in 32 patients with chronic persistent hepatitis (CPH), chronic active hepatitis (CAH) and liver cirrhosis (LC). Eleven patients had serum HBe antigen, 10 presented with HBe antibody and 11 had non-A, non-B hepatitis. IgG synthesis of PBMC induced with the two stimuli was significantly decreased in patients with CAH and LC when compared with that of controls. However, the generated amounts of IgG were not associated with the HB virus carrier state. B cells and T4+ cells were responsible for the diminished IgG synthesis in patients with CAH and LC when assessed by coculture experiments. On the other hand, proliferative response of PBMC to IL-2 and SAC were similar in controls and patient groups. These findings indicate that IgG production level of PBMC stimulated with IL-2 and SAC can reflect the severity of the underlying disease in chronic hepatitis patients.
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PMID:Proliferation and immunoglobulin synthesis of peripheral blood mononuclear cells from patients with chronic liver disease stimulated by Staphylococcus aureus Cowan 1 and interleukin 2. 311 35

To investigate mitogen induced helper interleukin 2 (IL-2) production in patients with chronic liver disease (CLD), IL-2 activity was assessed by an IL-2 bioassay using phytohaemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMNC). IL-2 activity was significantly reduced in patients with autoimmune chronic active hepatitis, primary biliary cirrhosis and alcoholic hepatitis with or without cirrhosis (P less than 0.01), and was comparable to controls in those with alcoholic cirrhosis alone. In vitro preincubation of PBMNC with lymphoblastoid alpha-interferon (alpha-IFN) before stimulation with PHA, led to a significant increase in IL-2 activity in all subjects (P less than 0.01), except those with alcoholic hepatitis, but in none of the groups did the levels of IL-2 activity reach those seen in normal subjects. The decrease in IL-2 activity in patients with CLD may be due to low IL-2 production or presence of an IL-2 antagonist(s). Such an abnormality may occur, not only as a result of liver damage, but may also be important in determining immunological disturbances involved in the pathogenesis of the liver disease.
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PMID:Interleukin 2 activity in chronic liver disease and the effect of in vitro alpha-interferon. 348 32

We investigated 37 patients with ascites and liver cirrhosis in order to examine whether on the basis of correlation of cytokines and acute phase proteins of the ascitic fluid, prognosis of spontaneous bacterial peritonitis can be made. Significantly enhanced levels of interleukin-6, as well as acute phase reactants alpha-1-antitrypsin and C-reactive protein were found in the ascitic fluid of patients with spontaneous bacterial peritonitis. The levels of tumour necrosis factor alpha (TNF-alpha), neopterin, interleukin 2-receptor and granulocyte-macrophage colony stimulating factor were higher in patients with spontaneous bacterial peritonitis, but without statistical significance, whereas no differences were found between the interferon gamma, interleukin-2 and interleukin-1 levels. In addition, interleukin-6, TNF-alpha and neopterin levels were found to correlate significantly with the outcome of the disease. These findings show that acute phase reaction occurs in the ascitic compartment in correlation with the development of spontaneous bacterial peritonitis.
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PMID:Spontaneous bacterial peritonitis is associated with high levels of interleukin-6 and its secondary mediators in ascitic fluid. 751 36

Approximately 5% of the world population is infected by the hepatitis B virus (HBV) that causes a necroinflammatory liver disease of variable duration and severity. Chronically infected patients with active liver disease carry a high risk of developing cirrhosis and hepatocellular carcinoma. The immune response to HBV-encoded antigens is responsible both for viral clearance and for disease pathogenesis during this infection. While the humoral antibody response to viral envelope antigens contributes to the clearance of circulating virus particles, the cellular immune response to the envelope, nucleocapsid, and polymerase antigens eliminates infected cells. The class I- and class II-restricted T cell responses to the virus are vigorous, polyclonal, and multispecific in acutely infected patients who successfully clear the virus, and the responses are relatively weak and more narrowly focused in chronically infected patients who do not. The pathogenetic and antiviral potential of the cytotoxic T lymphocyte (CTL) response to HBV has been demonstrated by the induction of a severe necroinflammatory liver disease following the adoptive transfer of HBsAg-specific CTL into HBV transgenic mice, and by the noncytolytic suppression of viral gene expression and replication in the same animals by a posttranscriptional mechanism mediated by interferon gamma, tumor necrosis factor alpha, and interleukin 2. The dominant cause of viral persistence during HBV infection is the development of a weak antiviral immune response to the viral antigens. While neonatal tolerance probably plays an important role in viral persistence in patients infected at birth, the basis for poor responsiveness in adult-onset infection is not well understood and requires further analysis. Viral evasion by epitope inactivation and T cell receptor antagonism may contribute to the worsening of viral persistence in the setting of an ineffective immune response, as can the incomplete downregulation of viral gene expression and the infection of immunologically privileged tissues. Chronic liver cell injury and the attendant inflammatory and regenerative responses create the mutagenic and mitogenic stimuli for the development of DNA damage that can cause hepatocellular carcinoma. Elucidation of the immunological and virological basis for HBV persistence may yield immunotherapeutic and antiviral strategies to terminate chronic HBV infection and reduce the risk of its life-threatening sequellae.
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PMID:Hepatitis B virus immunopathogenesis. 761 25


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