Apoptosis in the human liver during allograft rejection and end-stage liver disease

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Apoptosis in the human liver during allograft rejection and end-stage liver disease. / Afford, S C; Hubscher, S; Strain, A J; Adams, D H; Neuberger, J M; Adams, David.

In: Journal of Pathology, Vol. 176, No. 4, 08.1995, p. 373-80.

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@article{49a7e7c6b08a4558ab70fc8bb01e0cd1,
title = "Apoptosis in the human liver during allograft rejection and end-stage liver disease",
abstract = "The contribution of apoptosis (programmed cell death) to cellular damage in human liver disease is unknown. Using the in situ DNA end labelling method (ISEL), evidence was sought of programmed cell death (PCD) in liver tissue from patients with various liver diseases. In particular, the study aimed to determine whether PCD is involved in either the loss of interlobular bile ducts (vanishing bile duct syndrome--VBDS) or the perivenular hepatocyte drop-out, both of which are characteristic of irreversible graft rejection. Large numbers of apoptotic hepatocytes were found in perivenular areas in tissues taken from patients with chronic graft rejection. Significant hepatocyte apoptosis, was not seen in long-term stable allografts, primary biliary cirrhosis, cholestasis, paracetamol-induced fulminant hepatic failure, or fulminant hepatic failure of indeterminate origin (non-A, non-B, non-C hepatitis). Bile ducts rarely stained positively, but mononuclear cells present in the post-transplant tissues were frequently positive, showing nuclear or cytoplasmic staining. The presence of cytoplasmic staining suggested that some mononuclear cells had ingested apoptotic DNA from other cellular sources. PCD may thus contribute to the perivenular hepatocyte loss in chronic rejection. The absence of ductular epithelial cell staining suggests that PCD is not involved significantly in the bile duct loss of VBDS. Furthermore, apoptosis of mononuclear cells implies that PCD may be involved in regulating the inflammatory cell infiltration of graft rejection.",
keywords = "Apoptosis, Bile Ducts, Intrahepatic, Coloring Agents, Graft Rejection, Humans, Leukocytes, Mononuclear, Liver, Liver Diseases, Liver Transplantation",
author = "Afford, {S C} and S Hubscher and Strain, {A J} and Adams, {D H} and Neuberger, {J M} and David Adams",
year = "1995",
month = aug,
doi = "10.1002/path.1711760408",
language = "English",
volume = "176",
pages = "373--80",
journal = "Journal of Pathology",
issn = "0022-3417",
publisher = "Wiley",
number = "4",

}

RIS

TY - JOUR

T1 - Apoptosis in the human liver during allograft rejection and end-stage liver disease

AU - Afford, S C

AU - Hubscher, S

AU - Strain, A J

AU - Adams, D H

AU - Neuberger, J M

AU - Adams, David

PY - 1995/8

Y1 - 1995/8

N2 - The contribution of apoptosis (programmed cell death) to cellular damage in human liver disease is unknown. Using the in situ DNA end labelling method (ISEL), evidence was sought of programmed cell death (PCD) in liver tissue from patients with various liver diseases. In particular, the study aimed to determine whether PCD is involved in either the loss of interlobular bile ducts (vanishing bile duct syndrome--VBDS) or the perivenular hepatocyte drop-out, both of which are characteristic of irreversible graft rejection. Large numbers of apoptotic hepatocytes were found in perivenular areas in tissues taken from patients with chronic graft rejection. Significant hepatocyte apoptosis, was not seen in long-term stable allografts, primary biliary cirrhosis, cholestasis, paracetamol-induced fulminant hepatic failure, or fulminant hepatic failure of indeterminate origin (non-A, non-B, non-C hepatitis). Bile ducts rarely stained positively, but mononuclear cells present in the post-transplant tissues were frequently positive, showing nuclear or cytoplasmic staining. The presence of cytoplasmic staining suggested that some mononuclear cells had ingested apoptotic DNA from other cellular sources. PCD may thus contribute to the perivenular hepatocyte loss in chronic rejection. The absence of ductular epithelial cell staining suggests that PCD is not involved significantly in the bile duct loss of VBDS. Furthermore, apoptosis of mononuclear cells implies that PCD may be involved in regulating the inflammatory cell infiltration of graft rejection.

AB - The contribution of apoptosis (programmed cell death) to cellular damage in human liver disease is unknown. Using the in situ DNA end labelling method (ISEL), evidence was sought of programmed cell death (PCD) in liver tissue from patients with various liver diseases. In particular, the study aimed to determine whether PCD is involved in either the loss of interlobular bile ducts (vanishing bile duct syndrome--VBDS) or the perivenular hepatocyte drop-out, both of which are characteristic of irreversible graft rejection. Large numbers of apoptotic hepatocytes were found in perivenular areas in tissues taken from patients with chronic graft rejection. Significant hepatocyte apoptosis, was not seen in long-term stable allografts, primary biliary cirrhosis, cholestasis, paracetamol-induced fulminant hepatic failure, or fulminant hepatic failure of indeterminate origin (non-A, non-B, non-C hepatitis). Bile ducts rarely stained positively, but mononuclear cells present in the post-transplant tissues were frequently positive, showing nuclear or cytoplasmic staining. The presence of cytoplasmic staining suggested that some mononuclear cells had ingested apoptotic DNA from other cellular sources. PCD may thus contribute to the perivenular hepatocyte loss in chronic rejection. The absence of ductular epithelial cell staining suggests that PCD is not involved significantly in the bile duct loss of VBDS. Furthermore, apoptosis of mononuclear cells implies that PCD may be involved in regulating the inflammatory cell infiltration of graft rejection.

KW - Apoptosis

KW - Bile Ducts, Intrahepatic

KW - Coloring Agents

KW - Graft Rejection

KW - Humans

KW - Leukocytes, Mononuclear

KW - Liver

KW - Liver Diseases

KW - Liver Transplantation

U2 - 10.1002/path.1711760408

DO - 10.1002/path.1711760408

M3 - Article

C2 - 7562252

VL - 176

SP - 373

EP - 380

JO - Journal of Pathology

JF - Journal of Pathology

SN - 0022-3417

IS - 4

ER -