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)

Intravenous administration of soybean phosphatidylcholine liposomes containing different amounts of tocopherol acetate leads to a dose and time dependent increase of mouse liver tocopherol content, which was not observed when the preparation was given orally. When benzo[a]pyrene pretreated mice intoxicated with 400 mg/kg AAP were pretreated 2 h before with 1 g/kg phosphatidylcholine liposomes containing 4 mg/kg vitamin E acetate, these animals were protected against liver damage. Vitamin E alone or liposomes lacking vitamin E showed no protection. In an inflammatory liver disease model, i.e. fulminant hepatitis induced by intraperitoneal administration of 700 mg/kg galactosamine and 1 microgram/kg lipopolysaccharide phosphatidylcholine liposomes protected at a dose of 1 g/kg i.v. In this case, however, the protection was not due to the presence of vitamin E. These findings demonstrate the usefulness of phosphatidylcholine for liver protection and show that the protective spectrum is improved when they contain vitamin E. The data suggest that phosphatidylcholine is an excellent carrier for delivery of vitamin E to the liver.
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PMID:Hepatic uptake and antihepatotoxic properties of vitamin E and liposomes in the mouse. 236 59

The possible involvement of tumor necrosis factor-alpha in the pathogenesis of an experimentally induced hepatitis was investigated. Balb/c mice were primed with Propionibacterium acnes to induce the infiltration of mononuclear cells into the liver. Immunohistochemical study showed that most of the accumulated mononuclear cells at 7 days were Mac-2 positive, suggesting that they were activated macrophages. An injection of lipopolysaccharide resulted in massive hepatic necrosis and high mortality in the mice within 24 hours. Plasma tumor necrosis factor-alpha activity initially rose sharply and then declined over 3 hours. The increase in plasma aminotransferase activity correlated well with the elevation of plasma tumor necrosis factor-alpha activity. Pretreatment with dexamethasone or 16,16-dimethyl-prostaglandin E2 attenuated not only the elevation of plasma tumor necrosis factor-alpha activity but also the increase in plasma aminotransferase activity and improved the survival rate. Passive immunization against tumor necrosis factor-alpha showed protective effects. These findings suggest that tumor necrosis factor-alpha released from activated macrophages may play a crucial role in the pathogenesis of this murine hepatitis.
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PMID:Involvement of tumor necrosis factor-alpha in the pathogenesis of activated macrophage-mediated hepatitis in mice. 200 20

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

Mouse Hepatitis Virus type 3 (MHV3) multiplication in isolated murine Kupffer cells was partially inhibited by pretreatment of the cells with lipopolysaccharide (LPS). Supernatants of LPS-treated Kupffer cells contained large amounts of interferon. Inhibition of MHV3 multiplication was also observed when normal Kupffer cells were cultivated in a medium containing supernatants of LPS-treated Kupffer cells. In addition to the antiviral effect of the released interferon, there seems to be another effect of LPS, since Kupffer cells cultured in medium containing anti-interferon alpha beta antibodies were partially activated by LPS to inhibit MHV3 replication. The in vivo consequences of these effects for the local immunity of the liver against MHV3 infection are discussed.
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PMID:Inhibition of mouse hepatitis virus type 3 multiplication in activated Kupffer cells. 242 74

Resistance of mice to mouse hepatitis virus type 3 (MHV3) infection is genetically determined. Normal adult A/J mice are resistant, and BALB/c mice are susceptible. Higher titers of virus and interferon (IFN) in vivo were found in MHV3-infected BALB/c mice compared with A/J mice. In vitro activation of macrophages (M phi) by lipopolysaccharide (LPS) delayed MHV3 replication only in cells that originated from A/J mice, although cell populations from both A/J and BALB/c mice were able to synthesize comparable amounts of IFN-alpha/beta. Using specific antibodies, we have shown that the delayed MHV3 replication in LPS-activated A/J M phi was due, in part, to IFN-alpha/beta. A/J M phi were found to be more sensitive to IFN-gamma than to IFN-alpha/beta, and BALB/c M phi did not develop an antiviral state to either IFN. Cultured spleen cells from A/J mice synthesized more IFN-gamma than BALB/c spleen cells after specific or non-specific stimulation. The results indicate that IFN-activated M phi may play a crucial role in the resistance to MHV3 infection. Since IFN-gamma is produced in large amounts by A/J spleen cells after specific stimulation with MHV3 and is efficient in activating the A/J M phi, a T cell-dependent mechanism is likely to be involved.
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PMID:A major role of macrophage activation by interferon-gamma during mouse hepatitis virus type 3 infection. I. Genetically dependent resistance. 256 Apr 61

An important role in the endotoxin immobilization and transport from the intestine into the portal circulation belongs to the granulocytes which are likely able to transfer lipopolysaccharide to Kupffer cells. If the endotoxin diffusion into the mesenterial microvessels increases and (or) the portal circulation speed decreases, the interaction of lipopolysaccharide with granulocytes may become irreversible and facilitate the development of the systemic endotoxemia and the leucocyte-mediated liver damage. Intestinal flora endotoxin takes part in the liver damage pathogenesis in various forms of hepatitis, cirrhosis in various forms of hepatitis, cirrhosis and conditions followed by the circulation deficiency.
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PMID:[Endotoxin of intestinal microflora in liver pathology]. 268 96

Peripheral blood lymphocytes (PBLs) from a wild-caught woodchuck (WC192) chronically infected with woodchuck hepatitis virus (WHV) carried low levels of nonreplicating WHV genomes. In a previous study, these WHV genomes were induced to replicate and intact WHV particles were released when these PBLs were cultured in the presence of the generalized mitogen, lipopolysaccharide (LPS). To determine whether the culture-derived WHV particles were infectious, adult woodchucks were inoculated with cell-free culture medium from either LPS-stimulated or unstimulated WC192 PBLs. None of three animals inoculated with medium from the unstimulated PBL cultures developed positive WHV serologic markers or elevated liver enzyme levels during a 42-w observation period. In contrast, all three animals that received medium from the LPS-stimulated cultures displayed serologic markers of acute WHV infections 8-10 w after inoculation at up to a 100-fold dilution of the original culture medium. One of the three infected animals developed an acute hepatitis coincident with the appearance of the WHV markers. These results demonstrate that the WHV particles released from LPS-stimulated WC192 PBLs in culture are mature, infectious virions that also cause liver disease. Thus the LPS-induced replication of WHV in these cell cultures represents a transition from a latent to productive viral infection.
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PMID:In vitro production of infectious woodchuck hepatitis virus by lipopolysaccharide-stimulated peripheral blood lymphocytes. 279 56

The genetic sensitivity of mouse strains to mouse hepatitis virus 3 (MHV 3) has been related in vitro to a delay of virus replication in liver sinusoidal cells. In vivo immuno-histochemical studies of the liver from infected mice have demonstrated that mechanisms other than direct viral injury are in operation. To examine potential mechanisms, the interaction of lipopolysaccharide (LPS)-stimulated Kupffer cells with MHV 3 was studied. We first observed a dramatic inhibition in viral replication in LPS-treated Kupffer cells explanted from A/J resistant mice. Second, we demonstrated that MHV 3 induced a dose-dependent interleukin 1 (IL-1) activity in the supernatants of infected Kupffer cells of both strains. These results led us finally to examine the antigen-processing function of the Kupffer cells of both strains of mice. No striking differences were observed in the ability of Kupffer cells from resistant or sensitive mice to collaborate with immunocompetent lymphocytes. Our data suggest that Kupffer cells play a double role which is crucial in the pathogenesis of MHV 3-induced hepatitis. First, they act directly as the genetically determined sensitivity of mice to MHV 3 infection is correlated with the efficiency of the antiviral activity induced in Kupffer cells by LPS. Second, they act indirectly through the synthesis of different amounts of IL-1 induced by MHV 3. This hypothesis is further borne out by the effects of indomethacin treatment on the course of MHV 3 infection in A/J resistant mice in vivo.
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PMID:Interaction of mouse hepatitis virus 3 with Kupffer cells explanted from susceptible and resistant mouse strains. Antiviral activity, interleukin-1 synthesis. 285 6

Resistance to mouse hepatitis virus (MHV) in C3H mice is a genetic trait which appears 3-4 weeks after birth. However, when these animals were weaned on a low protein diet (8% casein), they remained susceptible to MHV-2 infection until they reached 8-9 weeks of age. During this period, the protein-restricted C3H mice were as susceptible to MHV-2 as the genetically susceptible congenic C3Hss strain. The delay in the emergence of resistance in the protein-restricted mice could be corrected by injecting these animals with spleen cells from 6-week-old C3H mice. Thymocytes from normal C3H mice, and splenocytes and thymocytes from protein-restricted C3H mice, were not protective. However, spleen cells from the protein-restricted mice were more responsive to phytohaemagglutinin, lipopolysaccharide and concanavalin A than spleen cells from normal C3H. The enhanced lymphoproliferative response in spleen cells from protein-restricted mice was abrogated by the addition of plastic-adherent cells obtained from normal C3H spleens. Spleen cells from protein-restricted and from genetically susceptible C3Hss mice also possessed more spontaneous cytotoxicity against MHV-infected 3T3 fibroblasts.
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PMID:Influences of nutrition on immunity and susceptibility to mouse hepatitis virus type 2. 299 Nov 26

The pore-forming protein, lipopolysaccharide-protein complex and lipopolysaccharide of Y. pseudotuberculosis outer membrane have been shown to participate in the penetration of the bacteria into the cells of the macroorganism, to produce a toxic effect on these cells and to enhance the ingesting activity of macrophages in small doses, while suppressing it in large doses. When introduced parenterally, protein induces a more pronounced clinical picture of specific reactive hepatitis in experimental animals and greater changes in their kidneys than the lipopolysaccharide--protein complex.
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PMID:[Components of the outer membrane of Yersinia pseudotuberculosis and their role in the pathogenesis of pseudotuberculosis]. 301 47


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