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

Intracerebral infection of mice with the neurotropic JHM strain of mouse hepatitis virus usually results in a fatal encephalomyelitis. However, infection with the neutralization resistant mutant, 2.2/7.2-V-2, results in inflammatory cell infiltration of the central nervous system with no apparent clinical symptoms, while conferring resistance to subsequent challenge with a lethal dose of wild type JHMV. The mononuclear cells infiltrating the brains of JHMV variant 2.2/7.2-V-2 infected mice were isolated and characterized. Virus-specific T cells which proliferated in response to JHMV antigen and produced both IL-2 and IFN-g were present among mononuclear cells infiltrating the brain as early as day 5 post-infection. The results suggest that the local immune response within the CNS may be important in dictating the outcome of disease following infections with neurotropic viruses.
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PMID:Virus-specific T cells in the central nervous system following infection with an avirulent neurotropic mouse hepatitis virus. 133 91

Male NMRI or BALB/c mice developed severe liver injury as assessed by transaminase release within 8 h when an intravenous dose greater than 1.5 mg/kg concanavalin A (Con A) was given. Histopathologically, only the liver was affected. Electron micrographs revealed leukocyte sticking to endothelial cells and bleb formation of hepatocytes. The hepatotoxicity of the lectin correlated neither with its agglutination activity nor with its sugar specificity. Administration of 0.5 mg/kg dexamethasone or 50 mg/kg cyclosporine A or 50 mg/kg FK 506 (Fujimycin) resulted in protection of the animals whereas indomethacin pretreatment failed to protect. Con A hepatitis was accompanied by the release of IL-2 into the serum of the animals. Mice with severe combined immunodeficiency syndrome lacking B as well as T lymphocytes were resistant against Con A. Athymic nude mice with immature T lymphocytes were also resistant. Pretreatment of mice with an antibody against T lymphocytes fully protected against Con A as did monoclonal anti-mouse CD4. Monoclonal anti-mouse CD8 failed to protect. Pretreatment of mice with silica particles, i.e., deletion of macrophages, prevented the induction of hepatitis. These findings provide evidence that Con A-induced liver injury depends on the activation of T lymphocytes by macrophages in the presence of Con A. The model might allow the study of the pathophysiology of immunologically mediated hepatic disorders such as autoimmune chronic active hepatitis.
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PMID:A T cell-dependent experimental liver injury in mice inducible by concanavalin A. 163 8

T lymphocyte-mediated cytolytic immune reactions are considered a major cause of hepatocyte injury in chronic viral and autoimmune hepatitis. To further investigate local immune responses, we studied the expression of lymphocyte antigens and cell-cell interaction molecules known to be involved in effector-target cell interactions by light and electron microscopy in liver biopsy specimens from patients with chronic viral and autoimmune hepatitis. CD8+ lymphocytes were found to be the predominant population of cells in the inflammatory infiltrate in chronic hepatitis B and non-A, non-B hepatitis. In contrast, CD4+ cells constituted a comparably higher proportion of cells and were more numerous than CD8+ cells in chronic autoimmune hepatitis. In both viral and autoimmune hepatitis, a substantial portion of lymphocytes expressed activation antigens such as T11/3 (CD2R) and IL-2-R (CD25). Lymphocyte function-associated antigen-3 (CD58), which mediates lymphocyte adhesion and activation and is the natural ligand of the CD2/T11 lymphocyte surface receptor, could be demonstrated on endothelial cells and hepatocytes. Hepatocellular lymphocyte function-associated antigen-3 expression in chronic hepatitis showed membranous and cytoplasmic staining of hepatocytes and had a positive correlation with the degree of inflammatory activity. These results suggest that effector-target interactions between hepatocytes and lymphocytes mediated by the lymphocyte function-associated antigen-3/CD2 pathway play a role in chronic inflammatory liver disease. Possible functional consequences of this interaction include enhancement of antigen-specific immune reactions and antigen-independent mechanisms of T cell activation, which may contribute considerably to the degree of inflammatory activity and tissue damage in chronic hepatitis.
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PMID:Hepatocellular expression of lymphocyte function-associated antigen 3 in chronic hepatitis. 171 65

Out of 165 children presenting with renal pathology, HBV-infection was detected by RIA in 69.7% of children suffering from glomerulonephritis and in 30.8% of children with pyelonephritis. The infection manifested by the carriage of HBs-antigen and persistent hepatitis. Unlike the control group (without HBv-infection), in patients with HBv-infection, glomerulonephritis was characterized by the development of a prognostically unfavourable mixed form there of in children under 7 years, by rare cases of the onset of a complete remission consequent to immunosuppressive therapy, a decline of the level of serum IgG and the T lymphocyte count, a reduction of the helper/suppressor ratio to 1.21 at the expense of a decrease of the number of helpers, and a higher amount of lymphocytes expressing receptors to IL-2.
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PMID:[Hepatitis B infection and primary glomerulonephritis in children]. 175 29

Lymphocytic dipeptidylaminopeptidase IV (DP-IV; E.C.3.4.14.5.) is described as a marker enzyme of immunostimulant T-lymphocytes as well as functional characteristic of IL-2-producing cells. Mononuclear cells of periphere blood (MNC) were isolated by density gradient centrifugation followed by enzymcytochemical staining of DP-IV positive cells and measuring of DP-IV enzyme activity using chromogenic substrates. As relative sign of single cell DP-IV activity we calculated average DP-IV activities of DP-IV positive cells. Blood samples from 14 patients with acute virus hepatitis, 30 cases of chronic active liver disease, 61 cases with liver cirrhosis of various kind and 19 patients with fatty liver and toxic hepatitis were investigated. As standard of comparison we used a group of healthy blood donors. By this way significant differences of described DP-IV parameters between some groups of liver disease were evident. Using an aetiologic classification of investigated liver diseases we found highly significant increased single cell activities in hepatitis-B associated cases in comparison to remarkable lower lower values in autoimmune cases. Different hypothesis about changes of lymphocytic dipeptidylaminopeptidase IV as a part of disturbed immunoregulation in chronic liver diseases were discussed.
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PMID:[Dipeptidylpeptidase IV activity in human lymphocytes in hepatobiliary diseases]. 197 80

We found that susceptibility to Murine Hepatitis Virus, type 3 (MHV3)-induced paralysis is controlled by genes of the H-2 complex. In this article, we compared MHV3 antigen specific cellular reactions, in congenic mice harbouring different H-2 genes (or gene). In a first set of experiments, paralysis susceptible (B10.A x A/J)F1, partly susceptible (B10.AQR x A/J)F1 and resistant (B10.Q x A/J)F1 hybrids were infected with live MHV3. Three weeks or more post-infection (p. i.), the spleens and peritoneal exudate (PE) cells from the mice were put into culture. Killed MHV3 was added to cultures, and antigen specific lymphokine production and utilization were measured: IL-1 production by PE cells after 24 hr in culture, IL-2 production by splenocytes after 24 hr in culture, IL-2 utilization (as appraised by splenocyte proliferation) after 96 hr in culture. No clearcut difference, resulting from genetic disparity, could be observed in the antigen-specific responses. In a second set of experiments, mice were primed with ultra-violet radiation killed MHV3. In that case, increases of IL-1 production by PE cells, of IL-2 production by splenocytes and splenocyte proliferation were always observed, compared to PE cells and splenocytes from non-primed (control) donor mice. However, in latter case, addition of MHV3 antigen to cultures did not result in augmentation of antigen specific IL-2 production and utilization. Here again, no genetic effect was observed. We conclude from these results that MHV3 infection elicited strong lymphokine responses, but that antigen-specific IL-1 and IL-2 production did not correlate with the susceptibility to MHV3-induced paralysis.
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PMID:Lymphokine release as measurement of anti-mouse hepatitis virus type 3 (MHV3) cellular reactions in various mouse lines exhibiting differential susceptibilities to MHV3-induced paralysis. 198 53

Effects of various cytokines on the proliferation of mouse hepatocytes were investigated. Human recombinant IL-6 not only enhanced the proliferation of mouse hepatocytes in the presence of epidermal growth factor, but also without epidermal growth factor. However, other human or mouse cytokines such as recombinant IL-1, IL-2, IL-3, IL-4, IFN-beta and IFN-gamma, which are known to regulate immune responses and/or hematopoiesis, had no effect on the proliferation of hepatocytes. These results suggest that IL-6 plays a crucial role in regulating the regeneration of hepatocytes after hepatitis or partial hepatectomy.
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PMID:Effect of human recombinant interleukin-6 on the proliferation of mouse hepatocytes in the primary culture. 218 3

In this study, we have investigated whether lymphocyte growth from 196 liver transplant biopsies is correlated with the histologic diagnosis of graft rejection. One fragment of each biopsy was cultured in IL-2 to expand activated T cells, and the remainder of the biopsy was analyzed histologically. A significantly higher number of biopsies with rejection grew lymphocytes when compared to those biopsies showing no evidence of rejection (P = 0.009). Lower growth rates were observed with biopsies taken from patients on OKT3 therapy (12% vs. 29% from patients not on OKT3), so when the data were reanalyzed after omitting those biopsies we observed an even stronger correlation of growth with rejection (P = 0.001). In spite of the fact that hepatitis biopsies are also infiltrated by lymphoid cells, the frequency of lymphocyte growth (16%) was similar to that observed for the biopsies with no rejection or hepatitis (19%) and much lower than for biopsies with rejection (42%). Over all, 82% of the cultures tested were positive for donor PLT reactivity, suggesting that current culture conditions favor alloreactive lymphocyte proliferation. The size of the biopsy cultured was found to be an important factor in the propagation of biopsy-infiltrating lymphocytes. Only 25% of smaller (less than 3 mm long) biopsies with rejection grew lymphocytes compared to 91% of the large-sized biopsies (greater than 5 mm long). It is likely that culture techniques will need to be modified in order to successfully propagate infiltrating lymphocytes that recognize antigens other than alloantigens.
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PMID:Propagation of lymphocytes infiltrating human liver allografts. Correlation with histologic diagnosis of rejection. 230 Oct

The authors used Wenger's vegetative nervous balance factor analysis to measure vegetative nervous function of 75 patients with vertigo revealing enhancement of sympathetic nervous function. The proliferation activity of IL-2 receptor was determined by the amount of 3H-TdR incorporated cpm in the peripheral blood lymphocyte after exogenous IL-2 stimulation (Lymphocult-T). The authors used this technique to measure the activity of IL-2 receptor in 49 patients with hepatitis and vertigo. The results showed that the activity of IL-2 receptor in patients with or without vertigo was lower than the controls (P less than 0.001). And patients with vertigo showed lower activity of IL-2 receptor than that without (P less than 0.01). In these patients with asthenia-syndrome the activity of IL-2 receptor was lower than those with asthenia syndrome. The activity of IL-2 receptor in these patients with long course was lower than those with short course. The difference of sex and age was not significant. The above results suggest that "Wind" in TCM might be related to the enhancement of sympathetic nervous function and the activity of IL-2 receptor.
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PMID:[Vegetative nervous function and interleukin-2 receptor in patients with vertigo]. 237 96

Subtoxic doses of endotoxin (salmonella abortus equi lipopolysaccharide, LPS) (5 micrograms/kg i.p.) or tumor necrosis factor alpha (TNF alpha) (15 micrograms/kg i.v.) induced fulminant hepatitis within 8 hr, when mice had been sensitized by a subtoxic dose of D-galactosamine (700 mg/kg i.p.). LPS-treatment led to the release of TNF into the circulation, independently of the presence of D-galactosamine. The TNF-dependent development of hepatitis was accompanied by a severe lymphopenia and neutrophilia as assessed by leukocyte differential count. The total leukocyte count was not significantly affected. Lymphopenia and neutrophilia were induced by LPS or TNF alpha alone; however, the differential count was not influenced by D-galactosamine. A quantity of 260 micrograms/kg phorbol myristate acetate (PMA) i.p. or 5 micrograms/kg platelet activating factor (PAF) i.v. or 3.3 mg/kg N-formyl-methionyl-leucyl-phenylalanine methylester (FMLP) i.v. or 167 mg/kg zymosan i.v. also caused lymphopenia and neutrophilia in mice. However, none of these agents induced the production of systemic TNF and therefore failed to induce hepatitis in D-galactosamine-sensitized mice. In LPS-insensitive C3H/HeJ mice administration of LPS produced neither differential count changes nor hepatitis while both events were observed when TNF alpha was given. This shows that TNF alpha alone gives rise to lymphopenia/neutrophilia as well as hepatitis independent of LPS. When the action of TNF alpha was blocked by anti TNF alpha antiserum pretreatment of LPS-sensitive mice, the animals were protected against LPS-induced hepatitis. However, lymphopenia and neutrophilia still occurred to a similar extent. The involvement of a putative additional mediator of LPS-induced leukocyte alterations was checked. The findings suggest that this mediator, if present, is different from IL-1, IL-2, eicosanoids or superoxide. We conclude from our findings that changes in leukocyte numbers and composition following D-galactosamine LPS or D-galactosamine/TNF alpha administration is an epiphenomenon rather than a causal event of leukocyte stimulation in the process of inducing a fulminant hepatitis in mice.
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PMID:Leukocyte alterations do not account for hepatitis induced by endotoxin or TNF alpha in galactosamine-sensitized mice. 240 85


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