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)

The special features of liver sinusoidal endothelium (LSE) are crucial for normal liver physiology. Cirrhotic livers, especially in primary biliary cirrhosis (PBC), are characterized by transformation of the LSE into a continuous, vascular type. The transformation is important for disease progression and explains some of the pathological hallmarks of the cirrhotic liver. Here, we investigated the presence of liver sinusoidal endothelial cell (LSEC)-reactive autoantibodies (Abs) in the sera of patients with autoimmune liver diseases, and assessed the ability of these Abs to transform LSE into vascular endothelium. Compared to healthy individuals (9%), significantly higher numbers of patients with PBC (59%; P < 0.001) and autoimmune hepatitis (AIH) (32%; P < 0.05) had Abs against LSECs. Incubation of primary LSEC cultures with F(ab')(2) fragments of anti-LSEC Abs isolated from sera of patients with PBC and AIH, induced 1) cell surface expression of vascular endothelium-associated markers, CD31, and factor VIII-related antigen; 2) significant production of fibronectin, laminin and collagen type IV; 3) loss of fenestrae, formation of tight junctions and Weibel-Palade bodies. Deposition of immunoglobulins on LSECs were found in liver biopsies of AIH and PBC patients. Thus, anti-LSEC autoAbs transform LSE into a vascular type and may therefore play an important role in the development of hepatocellular failure and portal hypertension in PBC and AIH patients.
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PMID:Capillarization of hepatic sinusoid by liver endothelial cell-reactive autoantibodies in patients with cirrhosis and chronic hepatitis. 1450 37

Nine weaned Labrador Retriever puppies from a litter of 11 were presented with signs of acute central nervous system (CNS) disease that included ataxia and blindness. All puppies died. Gross examination of tissues from 2 puppies revealed regionally diffuse hemorrhages in the brain stem and swollen hemorrhagic lymph nodes. Light microscopic examination of hematoxylin and eosin-stained tissues showed numerous large, basophilic intranuclear inclusion bodies within CNS vascular endothelium and occasionally in individual hepatocytes. Immunohistochemical staining of the tissue was positive using an antibody against canine adenovirus-1. Virus isolation for infectious canine hepatitis virus was achieved using inoculated cell cultures. Polymerase chain reaction amplification of DNA from cell culture material revealed shared homology with other mammalian adenoviruses.
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PMID:Diagnosis of infectious canine hepatitis virus (CAV-1) infection in puppies with encephalopathy. 1569 Sep 52

Targeting of the endothelial inflammatory adhesion molecule E-selectin by magnetic resonance imaging (MRI) was performed with a superparamagnetic contrast agent in the context of in vitro and in vivo models of inflammation. The specific contrast agent was obtained by grafting a synthetic mimetic of sialyl Lewis(x) (sLe(x)), a natural ligand of E-selectin expressed on leukocytes, on the dextran coating of ultrasmall particles of iron oxide (USPIO). This new contrast agent, called USPIO-g-sLe(x), was tested, in vitro, on cultured human umbilical vein endothelial cells (HUVECs) stimulated to express inflammatory adhesion molecules, and in vivo, on a mouse model of hepatitis. In vitro, HUVECs were stimulated with the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) and were then incubated with USPIO-g-sLe(x) or ungrafted USPIO. In vivo, hepatitis was induced on NMRI mice by injection of concanavalin A (Con A). USPIO-g-sLe(x) and ungrafted USPIO were injected intravenously. In vitro results showed an extensive retention of USPIO-g-sLe(x) on TNF-alpha stimulated HUVECs. Image intensity and R(2) measurements performed on T(2)-weighted MR images demonstrated a significantly higher binding of USPIO-g-sLe(x) on stimulated HUVECs. In vivo, USPIO are known to pass through the fenestrae of the liver and to be captured by Kupffer cells, inducing a loss of signal intensity on T(2)-weighted MR images. Unexpectedly, when injected to Con A-treated mice, USPIO-g-sLe(x) induced a significantly lower attenuation of liver signal intensity than USPIO or USPIO-g-sLe(x) injected to healthy mice, or USPIO injected to Con A-treated mice, suggesting that the specific contrast media is retained extracellularly by an interaction with E-selectin overexpressed on the vascular endothelium. Both in vitro and in vivo results therefore indicate that USPIO-g-sLe(x) is recognizing endothelial E-selectin. USPIO-g-sLe(x) is thus well suited for the MRI diagnosis of inflammation and for the in vitro evaluation of endothelial cells activation.
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PMID:Specific E-selectin targeting with a superparamagnetic MRI contrast agent. 1719 96

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease, where vascular lesions are one of the typical symptoms. The pathological process often involves skin vessels, renal glomeruli, the cardiovascular system, brain, lung alveoli, and gastrointestinal tract vessels. This review presents possible adverse mechanisms underlying the cause and effect relationship of various factors causing vascular lesions in SLE patients. The generally accepted hypothesis links vascular damage in SLE with the deposition of immune complexes in the vascular endothelium. The anti-endothelial cell antibodies (AECA), antiphospholipid antibodies and anti-double stranded DNA antibodies present in SLE, that directly or indirectly affect endothelial cells, causing inflammatory damage to the vessel wall, and their role, have been discussed. It has been stressed that although the suggested role of AECA in vasculitis pathogenesis has not been fully established, evidence, however, has demonstrated that AECA is a factor causing endothelial damage in SLE patients. On the other hand, issues concerning cellular adhesion molecules which enable leukocyte adhesion and rolling along the endothelial cell surface, and their extravascular migration, focus on the role they may be playing in SLE patients with vasculitis. A potential role of soluble forms of adhesion molecules, pentraxin 3, medications, infections in the pathogenesis of this disease has also been shown. Special attention has been given to the role of type 3 hepatitis virus in vascular damage in SLE.
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PMID:Vasculopathy and vasculitis in systemic lupus erythematosus. 1840 74

One difficulty in studying dengue virus (DENV) is the lack of an experimental model that reproduces the human disease. In a previous work, we have shown that BALB/c mice intraperitoneally inoculated with a DENV-2 isolate presented viremia and mild focal areas of liver injuries. In this study, mice were inoculated by the intravenous route and presented extensive damage areas in the liver tissue, which were evaluated by histopathological and ultrastructural analysis. Hepatic injury was noted mainly around the central vein and portal tracts. Damages consist of hepatocyte injury, including steatosis, swelling and necrosis. Further, erythrophagocytosis, intercellular edema and vascular damages were evident, including hemorrhage, which is characteristic of the dengue-induced hepatitis in human liver. Hepatic lesions were already noted 2 days post infection (p.i.), although effects were more extensive after the seventh day p.i. An increase in alanine aminotransferase and aspartate aminotransferase serum levels was detected 7 and 14 days p.i., respectively, and had correlation to hepatic lesions. Alterations caused by the DENV infection were self-limiting, with a remarkable reduction of all liver damages 49 days p.i. Virus antigens were detected in hepatocytes, Kupffer cells and vascular endothelium, suggesting virus replication in these cells. In situ hybridization, using a probe that anneals in the virus negative RNA strand, showed positive reaction in hepatocytes and vascular endothelium cells of infected mice, thus confirming virus replication in such cells. In general, results revealed that this mouse model reproduces some histopathological effects observed in humans and supports previous findings indicating virus replication in the hepatic tissue.
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PMID:Hepatic damage associated with dengue-2 virus replication in liver cells of BALB/c mice. 1972 15

Acute Human Cytomegalovirus (HCMV) infection is an unusual cause of venous thromboembolism, a potentially life-threatening condition. Thrombus formation can occur at the onset of the disease or later during the recovery and may also occur in the absence of acute HCMV hepatitis. It is likely due to both vascular endothelium damage caused by HCMV and impairment of the clotting balance caused by the virus itself. Here we report on two immunocompetent women with splanchnic thrombosis that occurred during the course of acute HCMV infection. Although the prevalence of venous thrombosis in patients with acute HCMV infection is unknown, physicians should be aware of its occurrence, particularly in immunocompetent patients presenting with fever and unexplained abdominal pain.
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PMID:Acute cytomegalovirus infection as a cause of venous thromboembolism. 2495 38


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