PubMed Health⌕ Search

Biomedical subjects

U Hopf

Publications and source records attributed to U Hopf.

At least 109 records · Page 6Linked to original sources
PubMed1990

Antibody activity against lipopolysaccharides, lipid A and proteins from Enterobacteriaceae in patients with chronic inflammatory liver diseases.

These studies are concerned with detection of circulating antibodies against various defined enterobacterial antigens in patients with chronic inflammatory liver diseases such as chronic hepatitis type B (n = 46), chronic active hepatitis (CAH) of autoimmune type (n = 10), alcoholic cirrhosis (n = 24) and primary biliary cirrhosis (PBC) (n = 24) as well as in healthy individuals (n = 39). Anti-LPS and anti-lipid A were determined by hemolytic and hemagglutination assay. Immunoblot technique was used to investigate the antibody activity against plasmid encoded proteins from Yersinia enterocolitica. Persistent titers of anti-LPS up to serum dilution 1:32.768 were found with hemolytic and hemagglutination assay in patients with alcoholic cirrhosis or PBC and in healthy control. In contrast nearly 50% of patients with chronic hepatitis B had no hemolytic antibodies against the two LPS E. coli serotypes at the time of liver biopsy. Anti-lipid A was detectable in 58% of patients with alcoholic cirrhosis but in low titers in less than 10% in the other groups (p less than 0.001). Alcoholic cirrhosis was also associated with a high frequency of IgG and IgA antibodies against plasmid encoded proteins from Yersinia enterocolitica. The data indicate that the O-polysaccharides as strong antigens are physiologically exposed to the immune system while lipid A and enterobacterial proteins are solely immunogenic under abnormal conditions.

Adult↗
PubMed1990

Experimental liver membrane antibodies (LMA) and antibodies against "liver specific protein (LSP)"--a comparative in vitro study.

Experimental antisera against the 26 kD rat liver protein--recently defined as a target antigen of LMA--and against "LSP" were tested on tissue sections and isolated hepatocytes from rat as well as with a variety of subcellular fractions as antigens. Anti-26 kD protein resulted in sharp immunofluorescence staining of hepatocellular plasma membranes in liver sections and on isolated hepatocytes, while the antiserum did not react with intracellular structures and was also negative with tissue sections from kidney and heart. Anti-"LSP" stained the plasma membranes of isolated hepatocytes, the cytoplasma of liver and kidney sections as well as the connective tissue of heart sections. In Western blot studies anti-26 kD protein showed a single band at 26 kD when liver plasma membranes and soluble liver protein fractions were used as antigens; a weak reaction was observed with microsomes and soluble kidney protein fractions, but there was no reaction with mitochondria or soluble heart proteins. Anti-"LSP" reacted with various proteins of the subcellular fractions between 16 and 116 kD. The 26 kD protein was found in peak II of Sepharose 6B chromatography of soluble liver protein fractions but was absent in the "LSP" fraction (peak I). We conclude that experimental LMA and anti-"LSP" recognize different epitopes of the hepatocellular plasma membrane.

Animals↗
PubMed1990

Glycoproteins of rat liver plasma membranes: their hepatocellular, intestinal and renal expression in rat, rabbit and human.

Expression of six glycoproteins (Mr = 60,000 (gp 60), 80,000 (gp 80), 110,000 (gp 110), 120,000 (gp 120), 140,000 (gp 140), 160,000 (gp 160)) recently purified from rat liver plasma membranes (LPM) were compared in the liver, small intestine and kidney of the rat, rabbit and human. Immunoblotting studies with monospecific antisera showed that five of the six glycoproteins (gp 60, gp 80, gp 110, gp 120, and gp 140) were expressed not only in LPM of the rat but also in LPM from the rabbit and human with Mr corresponding to those of the glycoproteins isolated from the rat. In contrast, the glycoprotein gp 160 was only detected in rat liver. The same pattern of expression was found by immunofluorescence on isolated hepatocytes from the three species. In rat liver, the glycoproteins were localized primarily either in the bile canalicular domain (gp 80, gp 110, gp 120), or in the sinusoidal domain (gp 60, gp 140), or they were distributed over the whole hepatocellular surface (gp 160). In rat, but not in rabbit or human, the glycoproteins gp 110, gp 120 and gp 140 were also found in the small intestine localized either in the brush border membrane (gp 110, gp 120) or over the whole surface membrane of enterocytes (gp 140). Gp 120 was also detected in the luminal pole of tubular epithelial cells of rats kidney. The data show that LPM of different mammalian species share several common glycoprotein antigens. These glycoproteins, that are also partly expressed in extrahepatic tissues, may represent plasma membrane structures conserved among mammalian species.

Animals↗
PubMed1990

[Long-term treatment of cryptogenic hepatitis C using recombinant interferon alpha].

In a pilot study 15 patients with cryptogenic chronic hepatitis non-A, non-B received human recombinant interferon alpha (rIFNa) at a dosage of 5 million units 3 times per week for periods of up to 4 months, followed by an additional 4-month course of treatment with 2 million units 3 times per week after an observed reduction in serum aminotransferase levels. Ten of the 15 patients demonstrated antibodies to hepatitis C virus (HCV). Pretreatment histological examinations revealed evidence of chronic aggressive hepatitis in 12 patients, 4 with signs of cirrhosis, and chronic persistent hepatitis (CPH) in the remaining 3 cases. Normalization of serum aminotransferase levels was documented in 9 patients (7 anti-HCV-positive), and a significant reduction occurred in 2 additional anti-HCV-positive cases. Follow-up biopsy at 8 months in 7 of the 11 responders documented improved histological findings in every case. Five patients with CAH in the initial study had discrete residual portal inflammation or mesenchymal reaction in the second histological examination. Clinical follow-up is currently at 12 month, and 3 anti-HCV-positive responders have normal aminotransferase levels. The data show that a subset of patients with chronic hepatitis C will demonstrate remission of disease after an 8-month course of treatment with rIFNa.

Adult↗
PubMed1989

Relation between Escherichia coli R(rough)-forms in gut, lipid A in liver, and primary biliary cirrhosis.

Since antimitochondrial antibodies (AMA) specific to primary biliary cirrhosis (PBC) recognise enterobacterial proteins and can be induced by R(rough)-mutants of enterobacteriaceae a study was done to find out the prevalence of enterobacterial R-forms in stool samples of patients with chronic inflammatory liver diseases. Liver biopsy specimens were also examined for lipid A, a common antigenic component of the cell wall in gram-negative bacteria. In all stool samples from the 21 patients with PBC Escherichia coli R-forms constituted up to half of the total amount of E coli. In contrast E coli R-forms were detectable in the stools of only 1 healthy control (n = 20), and in 25% of patients with other cholestatic diseases (n = 10), chronic hepatitis type B (n = 15), type non-A, non-B hepatitis (n = 15), or chronic pancreatitis and fat malabsorption (n = 8). An immunoblot technique showed that E coli R-forms isolated from patients' stools contained PBC-specific AMA-reactive proteins with molecular weights of 70-80 kD and 50 kD. Deposits of lipid A, located primarily in the cytoplasm of hepatocytes, were found in 11 patients with PBC but not in the liver of patients with chronic viral hepatitis. Circulating antibodies against lipid A were found rarely and in low titres. The data support the hypothesis that intestinal enterobacterial R-forms are aetiologically important in PBC and that antigens released from the bacterial cell wall contribute to the pathogenesis of the disease.

Adult↗
PubMed1989

HBcAg expressed on the surface of circulating Dane particles in patients with hepatitis B virus infection without evidence of anti-HBc formation.

Circulating immune complexes composed of HBcAg and anti-HBc have been demonstrated recently in patients with hepatitis B virus replication. After dissociation of immune complexes by chaotropic ions, HBcAg was quantified radioimmunologically. In the present study, we describe 10 patients with hepatitis B virus replication, absent or delayed anti-HBc formation and exposed HBcAg in serum. Four of the 10 patients had acute hepatitis, and six patients had chronic persistent hepatitis. In seven of 10 patients, a secondary immune defect was apparent due to acquired immunodeficiency syndrome, leukemia, histiocytosis X, sarcoidosis or end-stage renal disease. Electron microscopy demonstrated that Dane particles from anti-HBc-negative patients were agglutinated after addition of monoclonal anti-HBc antibodies, whereas Dane particles from anti-HBc-positive sera did not show agglutination. Monoclonal HBsAg-specific antibodies aggregated Dane particles independent of the presence of anti-HBc. Circulating HBcAg was always associated with the Dane particle fraction after density gradient separation. Hepatitis B virus core proteins from patients with and without anti-HBc studied by immunoblotting after sodium dodecyl sulfate-gel electrophoresis showed identical patterns. Hepatocytes from anti-HBc-negative patients were positive for HBcAg but negative for immunoglobulin G by immunofluorescence technique. The data indicate that HBcAg may also be expressed on the surface of Dane particles, where it is commonly masked by anti-HBc.

Acute Disease↗
PubMed1989

[Indications and current developments in liver transplantation].

Today, liver transplantation has become a routine treatment in many centres and will be increasingly applied in the future. Principal indications for liver transplantation are endstage chronic liver diseases, namely cirrhoses of various origin, fulminant hepatic failure, metabolic liver disease, and rarely non-resectable malignant tumors of the liver. Clinical and biochemical parameters indicative of the indication for liver transplantation can be stated with greater confidence. Advances in organ preservation with a new cold storage solution (University of Wisconsin solution) and further refinements in surgical technique and immunosuppression with application of multimodal protocols have led to a one-year-survival rate of 70%-80% in experienced centers. Since October 1988, 32 patients underwent liver transplantation in Berlin, currently, 31 patients are alive, while one patient died due to systemic fungal infection.

Carcinoma, Hepatocellular↗
PubMed1989

[Hepatitis B in established cardiac cirrhosis--a rare indication for liver transplantation].

A 34 year old patient was diagnosed as suffering from congestive cirrhosis due to constrictive pericarditis 18 years ago. A terminal dystrophic episode of additionally acquired chronic aggressive hepatitis B led to rapidly progressive liver failure. Orthotopic liver transplantation was carried out. 10 months after transplantation the patient is alive and well. Presence of HBsAg and HBcAg can again be demonstrated in the liver graft, however, without histologic evidence of hepatitis. Problems of prognosis after liver transplantation for hepatitis B virus infection are discussed.

Adult↗
PubMed1988

Are antimitochondrial antibodies in primary biliary cirrhosis induced by R(rough)-mutants of enterobacteriaceae?

Antimitochondrial antibody (AMA)-positive serum samples from 45 patients with primary biliary cirrhosis (PBC) and AMA-negative serum samples from patients with chronic liver diseases, systemic lupus erythematosus, or rheumatoid arthritis were studied by an immunoblot technique with mitochondria from bovine heart and pig kidney and with several strains of gram-negative bacteria as antigens after separation by sodiumdodecylsulphate polyacrylamide gel electrophoresis. Serum from patients with PBC recognised up to three mitochondrial antigens with molecular weights of 70 kD, 50 kD, and 42 kD. Equivalent patterns were found with bands at 70-80 kD and 50-52 kD with Enterobacteriaceae as antigens. AMA-reactive polypeptides were localised in the ribosomal and membrane fractions from Enterobacteriaceae but differed from known outer membrane proteins. Conversely, PBC-specific mitochondrial antigens at 70 kD and 50 kD were recognised by rabbit antisera against Salmonella minnesota Rb and Rc mutants but not by antisera against wild-type Enterobacteriaceae. Absorption experiments and two-dimensional immunoblotting studies confirmed that mitochondria and gram-negative bacteria share identical PBC-specific determinants. It seems that PBC-specific antigens are expressed in gram-negative bacteria and that these antigens may be immunogenic in mutants with defective polysaccharide synthesis. The data support the hypothesis of a bacterial aetiology for PBC.

Adult↗
PubMed1988

Abnormalities of B cell activation and immunoregulation in patients with chronic inflammatory liver diseases.

The immunoglobulin production capacities of peripheral blood lymphocytes obtained from patients with various chronic inflammatory liver diseases and from normal individuals were compared. Using a reverse hemolytic plaque assay, immunoglobulin-secreting cells (ISC) were counted immediately after isolation (immediate ISC) and again after 6-day, in vitro cultivation without stimulant (spontaneous ISC) or in the presence of pokeweed mitogen, PWM (PWM-induced ISC). An increased number of immediate ISC were observed in patients with chronic active hepatitis (CAH) of the autoimmune type (n = 7) or with CAH type B (n = 32), probably reflecting a defect of the in vivo suppressor cell system as previously demonstrated. In vitro preincubation of cells with 5 x 10(-8) M prednisolone reduced the increase in the number of immediate ISC in patients with CAH of the autoimmune type. On the other hand, lymphocytes obtained from patients with CAH-type NANB (n = 9) and with primary biliary cirrhosis (PBC) (n = 12) showed an impaired capacity to generate ISC upon stimulation with PWM. Spontaneous ISC from patients' lymphocytes were not significantly different from those of normal individuals. Using allogeneic co-cultures with lymphocytes from normal individuals and from patients with CAH NANB hepatitis or primary biliary cirrhosis, we observed no increase in suppressor cell activity. Therefore, the diminished responses to PWM are probably attributable to an alteration in the peripheral helper T-cell compartment.

Antibody Formation↗
PubMed1988

The significance of high-density lipoproteins (HDL) in the clearance of intravenously administered bacterial lipopolysaccharides (LPS) in mice.

The direct immunofluorescence technique was used to study the presence of high-density lipoproteins (HDL) in the liver, spleen and kidney of mice before and after intravenous administration of purified lipopolysaccharides (LPS) from Escherichia coli O 75, Salmonella abortus equi and Salmonella minnesota R 595, as well as free lipid A. Untreated mice had small granules of HDL in the hepatocellular cytoplasm, which appeared more pronounced after oral administration of fat. After intravenous administration of LPS, hepatocellular HDL decreased continuously and was no longer visible 1 hour after injection of LPS or lipid A. Five to ten minutes after administration, smooth-form LPS were located in sinusoidal cells, and rough form LPS and lipid A were found in both parenchymal and nonparenchymal liver cells. All toxins were demonstrated in both cell populations 1-4 hours after injection. The spleen was free of HDL, while there was a strong uptake of LPS into the cells of the reticulo-endothelial system. The kidney of experimental mice had small HDL granules in the epithelial cells of the proximal tubules, with a tendency to move to the lumen 1 hour after LPS injection, while there was a transient granular deposition of LPS in the glomeruli. The results suggest that the early uptake of circulating LPS by cells of the reticulo-histiocytic system in liver and spleen, as well as by hepatocytes, is not mediated by HDL. However, HDL located in hepatocytes or present in the circulation of experimental mice seem to be eliminated through the bile and the urine, induced by LPS.

Animals↗
PubMed1988

[Frequency and clinical relevance of delta virus infection in HBsAg carriers in the Berlin area].

The frequency of delta virus infection, immunoserological parameters and degree of liver inflammation were studied in 190 HBsAg carriers in the Berlin area from 1976 to 1986. Delta infection was detected in one of 50 HBsAg carriers (2%) in the period from 1976 to 1980. In contrast 19 of 140 HBsAg carriers (14%) with delta infection were found in the period from 1981 to 1986. This group included 12 Germans, 5 Turks and 2 Italians. Only 6 of these subjects belonged to a so-called risk group: 3 drug addicts, 2 homosexuals and 1 hemophiliac. Eighteen of the 20 patients with HDV infection showed progressive liver disease in the follow-up period. Nine cases developed complete liver cirrhosis over five years. Variable transaminase levels and elevation of immunoglobulin G were recorded. Humoral autoimmune phenomena were rarely observed. The increasing frequency of HDV infection in the Berlin area is presumably related to tourism, national origin and membership in specific risk groups. The data in our study underline the importance of effective prophylaxis by active immunization with HBsAg vaccines.

Adult↗
PubMed1988

[Schoenlein-Henoch purpura in chronic HBsAG-positive hepatitis].

We report about a 40-year-old male patient suffering from a recurrent vasculitis with purpura since the age of 18. In 1983, a HBsAg-positive chronic active hepatitis with circulating immune complexes which contained HBsAg, immunoglobulin M and G as well as complement (C) was diagnosed. Serum and liver tissue were negative for HBcAg, HBeAg and hepatitis B virus (HBV) DNA; there was no evidence for HBV replication. HBsAg, IgM and C3 were demonstrable in the arteriolar walls of the skin. The results support the concept that complement activating immune complexes containing HBsAg and IgM anti HBs play a role in the pathogenesis of vasculitis as described here.

Adult↗
PubMed1987

Serological assessment of HBcAg and HBV DNA: its prognostic relevance in acute hepatitis B.

Treatment of serum precipitates with sodium thiocyanate in patients with hepatitis B virus (HBV) replication results in liberation of circulating hepatitis core antigen (HBcAg) which can be demonstrated radioimmunologically. Follow-up investigations were performed in 80 patients with acute hepatitis B. Sera were examined for HBcAg. HBV DNA and conventional HBV markers. At the time of admission to hospital 34 of 80 (42%) patients were HBeAg positive. Twenty-six (76%) of the 34 HBcAg positive patients were HBV DNA positive, and circulating HBcAg was detectable in 25 of 34 (73%) HBcAg positive cases. In patients with uncomplicated courses of acute hepatitis B the serological HBcAg assay and HBV DNA became negative 1 to 8 weeks before elimination of HBeAg and up to 12 weeks earlier than the sera became negative for HBsAg. Five patients (6%) showed transition to chronic hepatitis B with persistence of HBsAg, HBeAg, HBV DNA and HBcAg in serum. One patient with acute hepatitis B and development of chronic hepatitis suffered from acquired immunodeficiency syndrome and showed delayed formation of anti-HBc. In this case uncomplexed HBcAg was demonstrable during the acute phase of hepatitis B. With the appearance of anti-HBc HBcAg circulated in a complexed form. The data indicate that serological determinations of HBcAg and HBV DNA can serve as prognostic markers in the early phase of acute hepatitis B. The demonstration of uncomplexed HBcAg in serum of a patient with inadequate formation of anti-HBc supports the hypothesis that circulating HBcAg is usually complexed by specific antibodies.

Acute Disease↗
PubMed1985

[Immunoserologic differentiation of chronic cholestatic hepatitis. Significance of antimitochondrial antibodies and hepatic membrane antibodies].

In 22 of 45 patients with chronic cholestatic liver inflammation and humoral immune phenomena, followed over 15 years with at least one liver biopsy, there was the histological picture of primary biliary cirrhosis (PBC), stages I to IV, with constantly demonstrable antimitochondrial antibodies (AMA) of M2-type. In 12 patients there were signs of PBC and chronic active hepatitis (CAH) in the liver histology, and they were M2-positive. Six of them also had M4-antibodies and were thus classified as 'mixed form'. The other six were seropositive for liver-membrane antibodies (LMA) and (or) antinuclear antibodies (ANA) and thus demonstrated an overlap between PBC and autoimmune or lupoid CAH. In five patients there was autoimmune CAH of lupoid type, in four of them with LMA or ANA without M2- or M4-antibodies. The remaining six patients had pericholangitis with persisting ANA and increased serum concentrations of immunoglobulin M without M2- and M4-antibodies, as well as LMA. Clinically a nondestructive polyarthritis predominated without definite signs of collagenosis. The listed immunoserological parameters make it largely possible to differentiate classical PBC, mixed forms or overlap of PBC and CAH, autoimmune CAH and nonpurulent cholangitis of pericholangitic type.

Aged↗