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)

1. An injection of D-galactosamine (GalN) into mice together with a lipopolysaccharide (LPS or endotoxin), interleukin-1 (IL-1) or tumour necrosis factor (TNF), sensitized the mice and induced fulminant hepatitis with severe congestion resulting in rapid death. Since LPS and these cytokines induce ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) in the liver and spleen of mice, the effects of GalN on the induction of ODC and HDC in these organs were examined. 2. The induction of ODC by LPS, IL-1 or TNF was suppressed by GalN in the liver, and this suppression preceded the hepatic congestion. There was good agreement between the degree of hepatic congestion and the suppression of ODC induction by various amounts of GalN. The induction of ODC in the spleen was suppressed only at the highest dose of GalN examined. 3. GalN is known to deplete uridine 5'-triphosphate (UTP), resulting in the suppression of RNA and protein synthesis. An injection of uridine, the precursor of UTP, diminished the GalN-induced suppression of ODC induction by LPS and prevented the hepatic congestion and death. 4. LPS-pretreatment before injection of LPS plus GalN prevented the suppression of ODC activity and prevented the hepatic congestion and death. 5. An injection of putrescine, the product of ODC, prolonged survival time and delayed the development of hepatic congestion. However, injection of an ODC inhibitor into the mice given LPS did not produce hepatic congestion. 6. The induction of HDC in the liver by LPS, IL-1 or TNF was not suppressed by GalN and, at high doses, the response to LPS was enhanced. An inhibitor of HDC neither prevented the hepatic congestion nor enhanced the protective effect of putrescine.7. Although GalN in combination with IL-la induced a markedly higher HDC activity than was observed when it was combined with TNFa, and suppressed the induction of ODC, the former combination at the doses used did not produce hepatic congestion or death. However, the sensitization to TNFa by GalN was markedly potentiated by IL-la.8. These results suggest that suppression of the induction of ODC by GalN may be one cause of the sensitization to LPS, IL-1 or TNF, and that the induction of HDC, i.e. histamine formation, may not be involved in this sensitization.9. These results are consistent with the hypothesis that both IL-1 and TNF are involved in the sensitization to LPS.
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PMID:Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin-1 or tumour necrosis factor by D-galactosamine. 147 81

Histamine is a classical, but still interesting inflammatory mediator. Many people have long believed that histamine is derived from mast cells or basophils alone. However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF). HDC is induced even in mast-cell-deficient mice. The histamine newly formed via the induction of HDC is released immediately and may be involved in a variety of immune responses. Reviewing our work and that of Schayer and Kahlson, the pioneers in this field, lead us to the conclusion that nowadays we need to understand that histamine can be produced via the induction of HDC by a mechanism coupled with the cytokine network. We call this histamine "neohistamine", to distinguish it from the classical histamine derived from mast cells or basophils. Neohistamine is involved in physiological reactions, inflammation, immune responses and a variety of diseases such as periodontitis, muscle fatigue (or temporomandibular disorders), stress- or drug-induced gastric ulcers, rheumatoid arthritis, complications in diabetes, hepatitis, allograft rejection, allergic reactions, tumor growth, and inflammatory side effects of aminobisphosphonates.
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PMID:[Induction of histidine decarboxylase in inflammation and immune responses]. 1149 27

Intragingival (ig) injection into mice of lipopolysaccharide (LPS) from Prevotella intermedia or Escherichia coli elevated the activity of the histamine-forming enzyme, histidine decarboxylase (HDC), in the mandible, liver, lung, and spleen, with a time course similar to that seen with intravenous (iv) injection. The effect of i.g. injection was less than that of i.v. injection but similar to that of intraperitoneal (ip) injection. The i.g. injection also increased hepatic serotonin, reflecting platelet accumulation. In galactosamine-treated mice, the minimum ig dose of LPS needed to induce lethal hepatitis was very small (less than that needed by ip injection). These results support the idea that the LPS produced in oral tissues may be transported easily to extraoral tissues and, in some cases, may cause inflammatory or immune responses. It also may influence the pathogenesis of some systemic diseases.
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PMID:Inflammatory reactions in extraoral tissues in mice after intragingival injection of lipopolysaccharide. 1174 Jul 32

Histamine is well known for its roles in allergic diseases and anaphylaxis through H(1)-receptor stimulation. The H(1)-receptor stimulation by histamine results in an increase in vascular permeability, vasodilatation, and stimulation of nerve terminals in primary sensory neurons, thereby accelerating the inflammatory responses. On the other hand, histamine has been demonstrated to be involved in the regulation of innate and acquired immune responses through H(2)-receptors. In a previous study with human peripheral blood mononuclear cells, we observed that histamine exerts various regulatory effects on monocyte/macrophage function. In this review, we discuss how inducible histamine protects mice from lethal hepatitis, induced by heat-killed P.acnes (1 mg, i.v.) followed by challenge with a low dose of lipopolysaccharide (1 microg), by reducing the excessive cytokine response in the liver. In addition, from in vivo studies with histidine decarboxylase knockout and H(1)-, H(2)-receptor knockout mice, the protective effect of histamine against fulminant hepatitis is shown to be elicited through H(2)-receptor stimulation.
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PMID:[Inducible histamine protects mice from hepatitis through H2-receptor stimulation]. 1823 72