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)

Activity of acid hydrolases, acid phosphatase, cathepsin D, DNA- and RNAases in lysosomal fractions of liver tissue and peripheric blood lymphocytes as well as concentration of circulating immune complexes in blood serum were studied in thymectomized rats and in thymectomized rats with chronic heliotrinic hepatitis; thymosin and alimentary factors were used for treatment and correction of the impairments observed. The rate of thymus hormones deficiency was found to be responsible for impairments of functional activity of lysosomes in lymphocytes and liver tissue. Activation of the lysosomal enzymes studied was detected within early periods (40 days) after thymectomy, while a decrease in the enzymatic activity was observed within later periods and to the end of the experiment (190 and 370 days). Besides, concentration of circulating immune complexes was increased in liver tissue and the most distinct increase occurred within 370 days after thymectomy. Activity of lysosomal enzymes in liver tissue and lymphocytes and content of circulating immune complexes in blood were normalized in thymectomized animals after treatment with thymosin and alimentary factors.
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PMID:[Change in the state of liver lysosomes and lymphocytes during development of secondary immunodeficiency and in chronic toxic hepatitis]. 837 13

The authors report an unusual case of herpes simplex type 2 (HSV) hepatitis which presented as part of a systemic HSV infection accompanied by disseminated intravascular coagulation (DIC). The patient was a 49-year-old Japanese male who three months prior to admission underwent surgical resection of his thymus for an invasive thymoma. Postoperatively, he received a course of chemotherapy which included prednisone, cyclophosphamide, vincristine, and pinorubicin. After discharge from the hospital, he was put on a maintenance dosage of prednisone and cyclophosphamide. Two weeks prior to this admission, the patient developed rhinorrhea, chills and general fatigue. Routine follow-up laboratory tests revealed markedly elevated liver enzymes which led to his immediate hospitalization. The tentative diagnosis on admission was fulminant hepatitis with DIC. The patient's condition steadily worsened during his hospitalization and acyclovir was initiated on the 4th hospital day due to the possibility of HSV hepatitis. He died on the same day. Histopathology performed on the liver at autopsy revealed hepatic inclusion bodies of HSV with positive immunohistochemical detection of the HSV type 2 antigen. Our case is the first report of HSV hepatitis associated with the removal of the thymus secondary to thymoma. It supports previous observations of disseminated HSV infection being prevalent in those patients with disorders of cell mediated immunity.
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PMID:Fatal herpes simplex hepatitis type 2 in a post-thymectomized adult. 848 19

The mechanism of CD11ahighCD8+ T cell induction after mouse hepatitis virus infection, which has been suggested to play a key role in the elimination of infectious virus from the spleen in C57BL/6 mice, was studied. In CD4+ T cell-depleted mice, CD11ahighCD8+ T cells were induced in the spleen and spleen cells showed virus-specific cytotoxic T lymphocyte activity after mouse hepatitis virus infection. The same results were obtained in adult thymectomized mice. These results indicate that CD11ahighCD8+ T cells can be generated after mouse hepatitis virus infection in the absence of either CD4+ T cells or the thymus.
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PMID:Generation of antiviral CD11ahigh T cells in CD4+ T cell-depleted mice and adult thymectomized mice after mouse hepatitis virus infection. 874 11

Thirty-five budgerigars were infected with the Psittacid herpesvirus 1 (RSL-1 strain, ATCC) to study the pathogenesis of Pacheco's disease. Intramuscular (i.m.) and oral (p.o.) infection routes were used in 21 and 14 animals respectively. Animals were euthanized on days 1, 2, 3, 4, 6 and 8 post-inoculation (p.i.) and complete postmortem examinations and histological studies were performed. The presence of viral antigen in tissues was detected by immunohistochemical techniques using a rabbit polyclonal antibody. In the i.m.-infected birds, lesions were first detected on the third day p.i. and included necrotizing hepatitis and splenitis, both associated to the presence of viral antigen. Necrotic and inflammatory lesions as well as viral antigen were detected in many organs after the fourth day p.i. (oesophagus, crop, pancreas, kidney, adrenal gland, thyroid and parathyroid glands, thymus, ovary and feathers) proving generalization of the disease. Chronology of the infection was similar in the p.o.-infected birds. However, two main differences were observed between the groups: In the p.o. group, viral antigen was first detected in cloacal mucosa (3rd day p.i.), liver and spleen; and viral entry into target cells and dissemination to the rest of the tissues was slower in this group. In addition, detection of viral antigen in feather follicular epithelial cells and in granulosa cells of organ follicles are findings that could be of relevance to the transmission of the virus.
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PMID:Immunocytochemical study of the pathogenesis of Pacheco's parrot disease in budgerigars. 891 50

Fas antigen (Fas/CD95) is a cell surface receptor protein that mediates apoptosis-inducing signals. To analyze the function of Fas in vivo, we examined the effects of agonistic anti-Fas antibodies in mice. The i.p. administration of the hamster anti-mouse Fas mAb, RK-8, which induced apoptosis both in vivo and in vitro, did not kill adult mice, whereas those given the another hamster anti-mouse Fas mAb, Jo2, rapidly died of fulminant hepatitis with hemorrhage. Histological analyses of mice given RK-8 indicated severe damage of the thymus, and moderate damage of the spleen and liver. Most of the thymocytes and some hepatocytes underwent apoptosis within 1 day of administration. Flow cytometry revealed that CD4+ T cells were more sensitive to Fas-mediated apoptosis than CD8+ T cells. At day 7 after administration, the thymus was atrophied. These in vivo effects of RK-8 were transient; the thymus was regenerated, and the liver and spleen were apparently normal 1 month after injection. The administration of RK-8 into newborn mice caused severe damage of the liver and thymus. Most of the hepatocytes died and jaundice was induced. The newborn mice died within 1 week. Most hepatocytes of newborn mice may be more sensitive to apoptosis-inducing signals through Fas than those of adult mice. These results indicated that functional Fas, which introduces the death signal in vivo, is expressed on thymocytes, CD4+ splenocytes, and some adult and most newborn mouse hepatocytes.
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PMID:In vivo analysis of Fas antigen-mediated apoptosis: effects of agonistic anti-mouse Fas mAb on thymus, spleen and liver. 904 12

We examined murine hepatitis virus strain A59 (MHV-A59)-induced demyelinating disease in C57BL/6 mice which had previously been thymectomized at 25 days of age. Demyelination was observed in 51-96% of spinal cord quadrants examined 30 or 60 days post infection (dpi), indicating that neither an intact thymus nor thymic infection is a prerequisite to demyelination. Depletion of CD4+ or CD8+ T cells at 5, 7 or 10 dpi did not influence the extent of demyelination indicating that neither T cell subset is a major effector of demyelination. However, these findings do not exclude the possibility that T cells are involved in initiating demyelinating disease very early in infection.
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PMID:CD4+ and CD8+ T cells are not major effectors of mouse hepatitis virus A59-induced demyelinating disease. 920 70

Mouse hepatitis virus, strain A59 (MHV-A59), is a coronavirus that triggers in susceptible mice a wide variety of pathologies, including hepatitis, thymus involution, B lymphocyte polyclonal activation and, after intra-cerebral inoculation, transient demyelination. One receptor that mediates entry of the virus into target cells has been identified: it is a glycoprotein of the carcinoembryonic antigen family, called Bgp1a. The availability of antibodies recognizing this molecule permits the analysis of its cellular expression and of the relationship between receptor expression and pathology induced by the virus. Bgp1a is found on epithelial and endothelial cells as well as on B lymphocytes and macrophages. In the liver, Bgp1a expression correlates well with infection of hepatocytes and endothelial cells, leading to the development of hepatitis. However, other cells expressing this molecule, such as central nervous system endothelial cells, are not infected by the virus. This observation may explain how the blood-brain barrier prevents dissemination of MHV-A59 from the general circulation into the brain. Thymic atrophy results from apoptosis of immature double-positive T lymphocytes which might be caused indirectly by infection of a small proportion of thymus epithelial cells that express Bgp1a rather than by infection of T cells that do not express the receptor. Finally, polyclonal activation of B lymphocytes, leading to increased secretion of antibodies of the IgG2a isotype, involves a cascade of events, including cytokine secretion, that may result from the interaction of MHV-A59 with B cells and macrophages that express Bgp1a. Therefore, after viral infection, cellular expression of Bgp1a may have different results: cell lysis; alteration of cellular functions that may lead to indirect death of other cell types, or resistance to infection.
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PMID:Morphological analysis of mouse hepatitis virus A59-induced pathology with regard to viral receptor expression. 947 48

Severe combined immunodeficient (SCID) mice accept human xenografts and can act as a model for human immune functions. Murine natural killer cells (NK), however, represent an important barrier for the reconstitution of SCID mice with human peripheral blood leukocytes (Hu-PBL). We investigated the effect on Hu-PBL survival of pretreatment with TM-beta1, a rat monoclonal antibody for the mouse IL-2 receptor beta chain. TM-beta1 greatly improved the survival of Hu-PBL. Human lymphocytes, predominantly T cells, survived in the peritoneum and infiltrated spleen and lungs already 1 week after engraftment and liver and thymus from 2 weeks on. Secondary humoral responses were evaluated with Hu-PBL from a donor immune to hepatitis-B surface Ag (HBsAg) and tetanus toxoid (TT). TM-beta1 pretreatment enhanced the recall Ig response to HBsAg and did not affect the baseline anti-TT Ig production. In conclusion, TM-beta1 pretreatment of SCID mice significantly improves the survival and functionality of the Hu-PBL graft.
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PMID:Murine IL-2 receptor beta chain blockade improves human leukocyte engraftment in SCID mice. 980 91

Mouse hepatitis virus (MHV) A59 infection which causes acute encephalitis, hepatitis, and chronic demyelination, is one of the experimental models for multiple sclerosis. Previous studies showed that lethal infection of beta2-microglobulin 'knockout' (beta2M(-/-)) mice required 500-fold less virus and viral clearance was delayed as compared to infection of immunocompetent C57Bl/6 (B6) mice. To investigate the mechanism of the increased susceptibility of beta2M(-/-) mice to MHV-A59, we studied organ pathology and the distribution of viral antigen and RNA during acute and chronic infection. A59-infected beta2M(-/-) mice were more susceptible to acute encephalitis and hepatitis, but did not have increased susceptibility to demyelination. Viral antigen and RNA distribution in the brain was increased in microglia, lymphocytes, and small vessel endothelial cells while the distribution in neurons and glia was similar in beta2M(-/-) mice and B6 mice. Acute hepatitis and thymus cortical hypoplasia in beta2M(-/-) mice were delayed in onset but pathologic changes in these organs were similar to those in B6 mice. The low rate of demyelination in beta2M(-/-) mice was consistent with the low dose of the virus given. A less neurotropic virus MHV-2, caused increased parenchymal inflammation in beta2M(-/-) mice, but without demyelination. Thus, CD8+ cells were important for viral clearance from endothelial cells, microglia and inflammatory cells, but not from neuronal and glial cells. In addition, CD8+ cells played a role in preventing the spread of encephalitis.
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PMID:Cellular reservoirs for coronavirus infection of the brain in beta2-microglobulin knockout mice. 1002 35

We have studied the susceptibility to infection by Mycobacterium lepraemurium (MLM) of a nude, hypothymic, CD1-derived, spontaneous mouse mutant called "et" because of its extraterrestrial appearance. We found that despite their hypothymia, et/et mice were not more susceptible to infection by MLM than their euthymic et/+ counterparts. Infection of both et/et and et/+ mice with 50 x 10(6) bacilli by the intraperitoneal route led only to a mild infection with low levels of antimycobacterial antibodies and a small number of lesions. These lesions were indicative of reactive hepatitis and hyaline perisplenitis with lymphoid hyperplasia. Some small bacilliferous granulomas were also observed at the end of the experiment (5 months of infection). CD1 mice behave in a rather "resistant" manner to the infection by MLM. It is clear that the nu gene is not necessarily linked to the thymus defect, and it is also clear that the hypothymia of et/et mice does not obviously affect their general cell-mediated immune competence.
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PMID:Susceptibility of "et," the spontaneously mutating CD1-derived nude mouse, to infection of M. lepraemurium. 1040 28


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