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)

Immunoregulatory function of peripheral blood monocytes was studied in patients with hepatocellular carcinoma (HCC) and liver cirrhosis (LC), by assaying interleukin 1 (IL-1) and prostaglandin E2 (PGE2) in the culture supernatant of lipopolysaccharide-stimulated monocytes. IL-1 activity of the monocyte culture supernatant without indomethacin was decreased in patients with HCC and LC, compared with that of controls. The activity was lower in patients with HCC than that in those with LC. The PGE2 content of the culture supernatant of monocytes from patients with LC and HCC was increased, compared to normal controls. To avoid the effect of PGE2 on the IL-1 assay, we cultured the monocytes with addition of indomethacin and assayed IL-1 activity in the culture supernatant. As a result, monocyte IL-1 production was increased in patients with HCC and LC, compared with normal controls. The decrease in IL-1 activity of the supernatant without indomethacin of patients with LC and HCC was considered to be due to increased secretion of PGE2 by the monocytes. Therefore, monocytes from patients with HCC and LC had an increased capacity of secreting both IL-1 and PGE2 over normal controls, but the effect of the suppressor function (PGE2 secretion) dominated in these patients.
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PMID:Decreased interleukin 1 activity in culture supernatant of lipopolysaccharide stimulated monocytes from patients with liver cirrhosis and hepatocellular carcinoma. 303 36

We investigated the role of interleukin 1 alpha (IL 1 alpha) in the pathogenesis of chronic liver disease. IL 1 alpha production by peripheral blood monocytes was measured with a specific, sensitive double-antibody radioimmunoassay. When monocytes were cultured for two days with bacterial lipopolysaccharide (LPS), IL 1 alpha production in asymptomatic hepatitis B virus carrier (ASC) and patients with chronic active hepatitis (CAH) was equivalent to that of controls (168 +/- 31 U/ml, mena +/- SD), while IL 1 alpha levels generated by monocytes from liver cirrhosis (LC) (117 +/- 45 U/ml, p less than 0.01) were significantly lower than controls. When normal monocytes were cultured together with LPS and IFN gamma, mena IL 1 alpha production was 297 +/- 56 U/ml. IL 1 alpha production in ASC did not differ from controls. On the other hand, IL 1 alpha production in patients with CAH (241 +/- 58 U/ml, p less than 0.05) and LC (189 +/- 70 U/ml, p less than 0.01) were significantly diminished in comparison with controls although there was considerable overlap. Serial study demonstrated that IL 1 alpha production rose significantly during acute deterioration of illness with marked rise in serum alanine aminotransferase. The addition of sera to normal monocytes cultures resulted in significantly enhanced suppression (p less than 0.05) for IL 1 alpha production in comparison with that of control sera. These findings indicate that decreased monocyte function and serum inhibitor(s) for IL 1 alpha production could contribute to the pathogenesis of chronic liver disease.
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PMID:Interleukin 1 alpha production by peripheral blood monocytes from patients with chronic liver disease and effect of sera on interleukin 1 alpha production. 314 31

Abnormalities of lymphocyte proliferation in chronic hepatitis B virus infection are well documented, although the underlying mechanisms are poorly understood. To determine whether these defects may be secondary to disordered lymphokine production, we have simultaneously assayed interleukin-1 and interleukin-2 production in 31 chronic carriers of the hepatitis B virus. Supernatants from mononuclear cells cultured both in the presence and absence of lipopolysaccharide contained significantly increased quantities of interleukin-1 activity in patients compared with normal controls (p less than 0.01). Lysates of monocytes from patients also contained more interleukin-1 than those of controls (p less than 0.05) in the presence of lipopolysaccharide or silica, or both. These results indicate that interleukin-1 production is markedly elevated in patients with chronic hepatitis B virus infection, whereas in contrast, interleukin-2 production was found to be reduced in these patients (p less than 0.01). As one of the biological properties of interleukin-1 is to stimulate fibroblasts to produce collagen, the relationship between fibrosis in the liver biopsy specimen and interleukin production was examined. There was a highly significant correlation (p less than 0.001) between interleukin-1 production and the severity of fibrosis, suggesting that this lymphokine may be closely related to the development of cirrhosis in such patients.
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PMID:Interleukin-1 and interleukin-2 activity in chronic hepatitis B virus infection. 325 34

Normal rats subjected to end-to-side portacaval shunt showed decreased survival and weight gain, a progressive fall in serum albumin and reciprocal rise in serum gamma globulin when compared with sham-operated controls for 12 weeks. Antibacterial lipopolysaccharide antibody was detected in significant titre at the sixth and twelfth weeks. It is suggested that the elevated levels of gamma globulin and reversal of albumin/globulin ratios noted in these animals may represent an immune response to bacterial lipopolysaccharides released into the systemic circulation as a result of the portacaval shunt. The hyperglobulinaemia of cirrhosis in human subjects may have a similar aetiology.
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PMID:Increased serum immunoglobulin levels following portacaval shunt in the normal rat. 413 11

We have developed a monocyte function test to determine the Interleukin 1 activity in lipopolysaccharide-stimulated monocyte culture supernatant, with or without the addition of indomethacin, in order to investigate helper and suppressor functions of monocytes in patients with chronic liver disease. Release of Interleukin 1 from monocytes was increased in patients with liver cirrhosis (p less than 0.01). Activity of suppressor monocytes was increased both in patients with chronic active hepatitis (p less than 0.01 and in those with liver cirrhosis (p less than 0.001). Since these disorders in the immunoregulatory function of monocytes were enhanced with advancement of liver dysfunction, we conclude that the liver plays an important role in maintaining normal monocyte function, and that chronic liver disease probably relates to dysfunction of monocytes.
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PMID:Interleukin 1 activity in culture supernatant of lipopolysaccharide-stimulated monocytes from patients with chronic liver disease. 633 23

Gram-negative bacterial infections are frequent and severe in cirrhotic patients. Existence of endotoxemia in cirrhosis is controversial. The demonstration of Gram-negative bacterial antibodies could be an alternative approach to the pathogenic role of these bacteria. In 58 patients with alcoholic cirrhosis, the immunoglobulin G specifically directed against the Gram-negative bacteria lipopolysaccharide expressed by the J5 mutant of Escherichia coli 0111:B4 was measured. Antibody titres were compared to those of a control group of blood donors. The distributions of antibody titres were similar in cirrhotic patients and in control subjects. No correlation was found between antibody titres and biological parameters of liver function. These results seem to confirm previous reports on the absence of latent endotoxemia in cirrhotic patients, and they suggest that antibody production against Gram-negative bacteria lipopolysaccharides is not enhanced in these patients.
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PMID:[Anti-Gram-negative bacterial antibodies in alcoholic cirrhosis. Study of 58 patients]. 674 68

Rats develop hyperglucagonemia after end-to-side portacaval shunt and also after splenocaval shunt. In this study, animals with mesocaval shunt were shown not to develop hyperglobulinemia or increased titers of lipopolysaccharide antibodies. It is currently thought that the hyperglobulinemia of cirrhosis results from diversion of immunogens past the liver into the systemic circulation with stimulation of sites of globulin synthesis. Since all procedures result in development of immune complexes in the systemic circulation, an alternative hypothesis was sought. It is proposed that the liver may regulate antibody production by the spleen but that this mechanism only operates if splenic venous blood passes through the liver. Portacaval shunt and splenocaval shunt result in diversion of splenic venous blood past the liver and, consequently, failure of regulation, while after mesocaval shunt, splenic venous blood still enters the liver and thus the regulatory mechanism could operate.
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PMID:Effect of mesentericocaval shunt upon globulin levels in the rat. 730 58

Murine macrophages express high levels of nitric oxide synthase and produce large amounts of nitric oxide (NO) when stimulated with certain cytokines in the presence of a trace amount of lipopolysaccharide (LPS). The stimulatory cytokines include interleukin-1 (IL-1), interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and migration inhibitory factor. Activated macrophages are highly effective killers of intra- and extra-cellular pathogens. However, as excessive NO can lead to immunopathology (diabetes, graft-v.-host disease, EAE, liver cirrhosis, rheumatoid arthritis), NO production is necessarily under tight regulation. A number of cytokines, including IL-4, IL-10 and transforming growth factor-beta, can down regulate the induction of NO synthase in macrophages. In addition, macrophages exposed to LPS alone and then stimulated with a mix of IFN-gamma and LPS express significantly lower levels of NO synthase than cells stimulated without pre-exposure to LPS. Furthermore, NO can reduce the activity of NO synthase by feedback inhibition, and also inhibit the production of IFN-gamma by Th1 cells (thus turning off its own synthesis from upstream). The regulatory pathways involve tyrosine kinase and protein kinase C.
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PMID:The role of nitric oxide in parasitic diseases. 751 Jan

Neopterin is produced by macrophages after stimulation with interferon gamma or lipopolysaccharide. Its production is increased in many infectious, autoimmune, and malignant diseases. The aim of this study was to examine whether, on the basis of neopterin as a marker, liver diseases could be classified according to aetiology and stage of disease. A cohort of 264 patients with chronic liver diseases (viral, metabolic, autoimmune, toxic) and 150 normal controls were studied; 136 of the patients had cirrhosis. Increased serum neopterin concentrations were found in 41% of all patients (controls 6.0 (2.2) nmol/l), with patients in the cirrhotic stage of disease showing higher neopterin values (mean (SD) 15.7 (23.6) nmol/ml) than those in the non-cirrhotic stage (9.9 (5.5)). There were no statistically significant differences in the serum neopterin concentrations that could be considered characteristic for different stages of disease classified according to the Child criteria. Such differences in concentrations of neopterin that were found in patients with liver diseases grouped according to underlying causes were only marginal. Serum neopterin concentrations were found to be significantly lower than in any other disease group only in patients with Wilson's disease. The results suggest that activated macrophages participate in the development of chronic liver disease. Measurement of serum neopterin does not offer a reliable method for differentiating between various aetiologies of chronic liver diseases and does not help to predict severity of cirrhosis.
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PMID:Serum neopterin concentrations in chronic liver disease. 767 57

Alveolar macrophages (AM) exposed to microorganisms secrete cytokines that are important to lung defense. Since alcoholic liver cirrhosis (ALC) patients are susceptible to lung infections, the ability of AM in such patients to produce the cytokines tumor necrosis factor-alpha, interleukin (IL)-1 beta, and IL-6 was evaluated by mRNA expression and protein secretion. Adherent AM from ALC and alcoholic patients and controls were cultured with and without lipopolysaccharide (LPS): Mean cytokine levels in ALC and alcoholic subjects were not significantly different than in controls. However, LPS-stimulated AM from 13 of 29 ALC patients exhibited a reduced ability, compared with that from controls, to secrete the cytokines (P < .05 for all 3). Specific mRNA expression was also impaired in the 13 patients, and their liver diseases were more severe than those of other patients. Impaired cytokine production by AM in ALC patients with severe cirrhosis may account for their increased susceptibility to lung infections.
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PMID:Impaired secretion and mRNA expression of monokines by alveolar macrophages from nonsmoking patients with alcoholic liver cirrhosis. 787 33


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