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J M Vierling

Publications and source records attributed to J M Vierling.

At least 55 records · Page 3Linked to original sources
PubMed1989

Hepatic homing of mononuclear inflammatory cells isolated during murine chronic graft-vs-host disease.

Liver injury in murine chronic graft-vs-host disease (CGVHD) to minor histocompatibility Ag, B10.D2----BALB/c (600 rad), is characterized by mononuclear cell inflammation and necrosis of interlobular bile ducts. Bile duct destruction in this model is similar to that which occurs in human CGVHD, late liver transplant rejection, and primary biliary cirrhosis. This model provides a unique opportunity to isolate mononuclear inflammatory cells from the liver during CGVHD, study their functions, and investigate the immunologic mechanisms responsible for bile duct destruction. In the present study, we compared the in vivo organ homing of mononuclear inflammatory cells (MC) isolated from the liver and spleen during the course of CGVHD. MC isolated from the liver showed a progressive increase in homing to the livers of BALB/c mice from day 7 through 42. In contrast, the hepatic homing of MC isolated from the spleen peaked at day 21 and subsequently declined. CGVHD spleen MC showed a progressive increase in homing to the spleen of BALB/c mice whereas CGVHD liver MC showed no change over time. Homing to other organs was negligible. The hepatic and splenic homing of MC isolated during CGVHD was significantly greater in BALB/c (host) mice than in B10.D2 (donor) mice. Autoradiography was used to determine the intrahepatic sites at which CGVHD liver MC accumulate after i.v. injection into BALB/c mice. The results indicated that MC isolated from the liver when bile duct inflammation is most intense accumulate preferentially in hepatic portal spaces in close proximity to interlobular bile ducts. These results suggest that hepatic homing by CGVHD liver MC is specific for minor histocompatibility Ag expressed on host biliary epithelial cells. These data support the hypothesis that bile duct destruction in murine CGVHD is mediated by MC that are sensitized to minor histocompatibility Ag expressed by host biliary epithelial cells.

Animals↗
PubMed1987

Transmission of hepatitis B virus by artificial insemination.

Although the capacity for transmission of hepatitis B infection by semen is well recognized, the potential for transmission by artificial insemination remains theoretical. Currently, screening of semen donors for hepatitis B virus infection is not standard practice. We saw a case of acute viral hepatitis B in a woman following artificial insemination with semen from a donor subsequently found to be positive for hepatitis B surface antigen (HBsAg). Both the donor serum and semen contained HBsAg and hepatitis B e antigen, and the HBsAg subtype was identical to that of the patient. Documentation of hepatitis B virus transmission by artificial insemination indicates that HBsAg screening of semen donors should be routine practice.

Adult↗
PubMed1987

Chyloperitoneum with collateral lymphatic drainage involving abdominal skin.

A 58-year-old man with poorly differentiated lymphoma and chyloperitoneum, who developed periumbilical white vesicular skin lesions, is presented. These skin lesions represent collateral lymphatic drainage pathways for the chyloperitonium as evidenced by drainage of chylous fluid from these lesions and communication with the peritoneum as demonstrated by intraperitoneal 99mTc sulfur colloid injection.

Abdomen↗
PubMed1987

Monoclonal antibodies identifying antigens on distinct domains of rat hepatocytes.

To aid in evaluating the functional significance of various domains of the hepatocyte plasma membrane, we have developed monoclonal antibodies that react with three different antigens on the surface of rat hepatocytes. One antigen is present on the sinusoidal-lateral plasma membrane but is absent from the bile canalicular membrane. On the basis of apparent molecular weight and ability to bind a desialylated glycoprotein, this antigen may be the asialoglycoprotein receptor. It was also identified immunocytochemically on the sinusoidal-lateral plasma membrane of human hepatocytes. The second antigen is present only on the bile canalicular membrane, whereas the third is present on the entire cell surface of rat hepatocytes. Our monoclonal antibodies may be useful in investigations of the sorting mechanisms of hepatocyte membrane proteins and the pathogenesis of certain liver diseases.

Animals↗
PubMed1985

Hepatic uptake and disposition of human polymeric IgA1 in perfused rat liver: evidence for incomplete biliary excretion and intrahepatic degradation.

The hepatic uptake of polymeric immunoglobulin A (IgA) is mediated by secretory component; the resulting secretory IgA is excreted intact into bile. To define the hepatic metabolism of polymeric IgA, we quantitated the uptake and transport of human polymeric IgA1 after a single pass through the perfused rat liver. Uptake of polymeric IgA1 was compared with that of asialoorosomucoid, a glycoprotein whose uptake is mediated by the asialoglycoprotein receptor. Single-pass hepatic uptake of 125I-polymeric IgA1 and of 125I-asialoorosomucoid averaged 18.0 +/- 3.1% (SE) and 71.8 +/- 2.8%, respectively. The uptake of 125I-polymeric IgA1 was inhibited by excess unlabeled polymeric IgA1 but not by asialoorosomucoid. Only 13.0 +/- 1.6% of the 125I-polymeric IgA1 extracted by the liver was excreted into bile, whereas three-fourths was released into the hepatic venous effluent in degraded form. Thus, both the uptake and biliary excretion of polymeric IgA1 by the rat liver are inefficient processes. Polymeric IgA1 follows two distinct pathways after uptake by the liver: a small proportion is excreted intact into bile, while the majority is degraded and released back into the circulation.

Animals↗
PubMed1985

Isolated perfusion of murine liver in situ: technique and validation.

Although liver perfusion in situ is a valuable technique for the study of hepatic metabolism, it has rarely been applied to the study of mice. This is primarily due to the lack of a simple, reproducible technique to cannulate the delicate portal vein and initiate perfusion without irreversible hepatic injury. Therefore, we developed a technique to overcome these obstacles and performed studies to assess the viability of the perfused murine liver. The inflow catheter assembly permits rapid, reproducible cannulation of the portal vein and protects the cannulated vein from the effects of subsequent manipulations. Serial assessments of perfusion pressure, flow rate, perfusate pH, oxygen consumption, and fluxes of alanine aminotransferase and potassium indicate that the murine liver remains viable during perfusion. Moreover, the light and electron microscopic appearance of perfused livers is indistinguishable from that of freshly excised control livers. This technique should facilitate perfusion studies of hepatic metabolism in murine strains with genetic homogeneity and defined genetic abnormalities of hepatic metabolism.

Alanine Transaminase↗
PubMed1984

Ultrastructural immunocytochemical localization of the asialoglycoprotein receptor in rat hepatocytes.

The asialoglycoprotein receptor is present on the plasma membrane of rat hepatocytes and mediates the endocytosis of exogenous asialoglycoproteins. The intracellular locations of the receptor are incompletely defined, and whether the receptor is present on the canalicular membrane is controversial. To investigate these unresolved issues, we localized the asialoglycoprotein receptor on the surfaces of and within rat hepatocytes in the absence of exogenous asialoglycoprotein. Cryostat sections of perfusion-fixed livers of fasted rats were incubated with peroxidase-labeled antibodies to the rat asialoglycoprotein receptor and were examined by light and electron microscopy. The asialoglycoprotein receptor on the surface of hepatocytes was present on the sinusoidal plasma membrane and was concentrated in coated pits; it was present also on the lateral plasma membrane but was absent from the bile canalicular membrane. Within hepatocytes, the receptor was present in saccules of the Golgi complexes and occasionally in segments of the endoplasmic reticulum. Definite endocytic vesicles containing receptor were absent, and lysosomes were devoid of the receptor. These observations indicate that in the absence of exogenous asialoglycoprotein (a) the asialoglycoprotein receptor on the plasma membrane of hepatocytes is present only on the sinusoidal and lateral surfaces, (b) the receptor is being synthesized and assembled, (c) endocytic internalization of the receptor is minimal or absent, and (d) lysosomes are devoid of the receptor.

Animals↗
PubMed1984

Cellular distribution of the asialoglycoprotein receptor in rat liver. Implications for hepatic accumulation of desialylated lymphocytes.

It has been postulated that the selective accumulation of circulating desialylated cells in the mammalian liver results from the binding of desialylated glycoproteins on surfaces of the cells to asialoglycoprotein receptors in the liver. Since circulating cells in the liver are in contact predominantly with sinusoidal lining cells (Kupffer cells and endothelial cells), this postulate requires the presence of asialoglycoprotein receptors on the luminal surface of the sinusoidal lining cells. Whether the receptor is present on these cells, however, remains controversial. To clarify this issue, we used an indirect immunoelectron microscopic method to determine the distribution of the receptor on the surfaces of hepatic cells accessible to the circulation. F(ab')2 fragments of antireceptor antibodies were perfused in situ via the portal vein prior to tissue fixation. After perfusion fixation, sections were reacted with peroxidase-labeled antibodies to the antireceptor F(ab')2. The plasma membranes of Kupffer cells, endothelial cells, and fat-storing cells were devoid of the asialoglycoprotein receptor. In contrast, the receptor was associated with hepatocytes, where it was present diffusely on the sinusoidal plasma membranes and concentrated within coated pits. We conclude that it is unlikely that circulating desialylated cells bind to the asialoglycoprotein receptor in the liver unless a breach in the continuity of sinusoidal lining cells exists.

Animals↗
PubMed1981

Effect of splenectomy of hepatic bilirubin clearance in patients with hereditary spherocytosis. Implications for the diagnosis of Gilbert's syndrome.

BRT and CBR were determined from studies of radiobilirubin kinetics in 14 patients undergoing splenectomy for hereditary spherocytosis. Studies were conducted both before and after the operation in order to assess the effects of the postsplenectomy fall in BRT on CBR. Splenectomy led to a doubling of the RBC-t1/2 from 13.0 +/- 1.7 (S.E.) days to 26.1 +/- 1.5 and a fall in BRT from 15.9 +/- 4.4 mg/kg/day to 4.3 +/- 0.9. In seven patients (group A) initially normal values for CBR were unaltered by surgery. In the remaining seven (group B), low preoperative values for CBR, suggestive of Gilbert's syndrome, uniformly improved after splenectomy, becoming normal in five patients. Nevertheless, family studies and reduced values for UDPGT activity supported the initial impression of concomitant Gilbert's syndrome in group B. These studies suggest the existence of a latent state for Gilbert's syndrome that, in some patients, may be unmasked by a hemolytic stress. As such, they have important implications for both pedigree analysis and incidence studies of this condition.

Adolescent↗