Expression of Fas Ligand by Hepatic Macrophages in Patients with Fulminant Hepatic Failure
The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement. The subjects were 24 patients with FHF wh...
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| Published in | The American journal of gastroenterology Vol. 100; no. 11; pp. 2551 - 2559 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Blackwell Publishing
01.11.2005
Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0002-9270 1572-0241 |
| DOI | 10.1111/j.1572-0241.2005.00265.x |
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| Abstract | The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement.
The subjects were 24 patients with FHF who underwent liver transplantation at our institution. For comparison, nine chronic hepatitis (CH) patients and six living liver donors (LD) were also enrolled. Liver tissues were obtained for histological (hematoxylin-eosin, terminal deoxynucleotidyl transferase [TdT]-mediated dUTP-biotin nick-end labeling [TUNEL], immunohistochemistry, and double immunofluorescence staining) and reverse transcription PCR (RT-PCR; cytokines and chemokines) analysis.
The numbers of TUNEL-, FasL-, and CD68-positive cells in the livers of patients with FHF were significantly larger than in those with CH or with normal livers. Double immunofluorescence staining showed that FasL was expressed predominantly on liver macrophages and rarely on CD8-positive lymphocytes. RT-PCR study showed increased expression of FasL; interferon-gamma; interleukin-18; macrophage inhibitory protein-1beta; and regulated upon activation, normal T cell expressed and secreted in the livers of patients with FHF compared with those of LD.
Macrophages and their expression of FasL may play roles in the pathogenesis of FHF. |
|---|---|
| AbstractList | OBJECTIVESThe mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement. METHODSThe subjects were 24 patients with FHF who underwent liver transplantation at our institution. For comparison, nine chronic hepatitis (CH) patients and six living liver donors (LD) were also enrolled. Liver tissues were obtained for histological (hematoxylin-eosin, terminal deoxynucleotidyl transferase [TdT]-mediated dUTP-biotin nick-end labeling [TUNEL], immunohistochemistry, and double immunofluorescence staining) and reverse transcription PCR (RT-PCR; cytokines and chemokines) analysis. RESULTSThe numbers of TUNEL-, FasL-, and CD68-positive cells in the livers of patients with FHF were significantly larger than in those with CH or with normal livers. Double immunofluorescence staining showed that FasL was expressed predominantly on liver macrophages and rarely on CD8-positive lymphocytes. RT-PCR study showed increased expression of FasL; interferon- gamma ; interleukin-18; macrophage inhibitory protein-1 beta ; and regulated upon activation, normal T cell expressed and secreted in the livers of patients with FHF compared with those of LD. CONCLUSIONSMacrophages and their expression of FasL may play roles in the pathogenesis of FHF. The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement.OBJECTIVESThe mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement.The subjects were 24 patients with FHF who underwent liver transplantation at our institution. For comparison, nine chronic hepatitis (CH) patients and six living liver donors (LD) were also enrolled. Liver tissues were obtained for histological (hematoxylin-eosin, terminal deoxynucleotidyl transferase [TdT]-mediated dUTP-biotin nick-end labeling [TUNEL], immunohistochemistry, and double immunofluorescence staining) and reverse transcription PCR (RT-PCR; cytokines and chemokines) analysis.METHODSThe subjects were 24 patients with FHF who underwent liver transplantation at our institution. For comparison, nine chronic hepatitis (CH) patients and six living liver donors (LD) were also enrolled. Liver tissues were obtained for histological (hematoxylin-eosin, terminal deoxynucleotidyl transferase [TdT]-mediated dUTP-biotin nick-end labeling [TUNEL], immunohistochemistry, and double immunofluorescence staining) and reverse transcription PCR (RT-PCR; cytokines and chemokines) analysis.The numbers of TUNEL-, FasL-, and CD68-positive cells in the livers of patients with FHF were significantly larger than in those with CH or with normal livers. Double immunofluorescence staining showed that FasL was expressed predominantly on liver macrophages and rarely on CD8-positive lymphocytes. RT-PCR study showed increased expression of FasL; interferon-gamma; interleukin-18; macrophage inhibitory protein-1beta; and regulated upon activation, normal T cell expressed and secreted in the livers of patients with FHF compared with those of LD.RESULTSThe numbers of TUNEL-, FasL-, and CD68-positive cells in the livers of patients with FHF were significantly larger than in those with CH or with normal livers. Double immunofluorescence staining showed that FasL was expressed predominantly on liver macrophages and rarely on CD8-positive lymphocytes. RT-PCR study showed increased expression of FasL; interferon-gamma; interleukin-18; macrophage inhibitory protein-1beta; and regulated upon activation, normal T cell expressed and secreted in the livers of patients with FHF compared with those of LD.Macrophages and their expression of FasL may play roles in the pathogenesis of FHF.CONCLUSIONSMacrophages and their expression of FasL may play roles in the pathogenesis of FHF. The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement. The subjects were 24 patients with FHF who underwent liver transplantation at our institution. For comparison, nine chronic hepatitis (CH) patients and six living liver donors (LD) were also enrolled. Liver tissues were obtained for histological (hematoxylin-eosin, terminal deoxynucleotidyl transferase [TdT]-mediated dUTP-biotin nick-end labeling [TUNEL], immunohistochemistry, and double immunofluorescence staining) and reverse transcription PCR (RT-PCR; cytokines and chemokines) analysis. The numbers of TUNEL-, FasL-, and CD68-positive cells in the livers of patients with FHF were significantly larger than in those with CH or with normal livers. Double immunofluorescence staining showed that FasL was expressed predominantly on liver macrophages and rarely on CD8-positive lymphocytes. RT-PCR study showed increased expression of FasL; interferon-gamma; interleukin-18; macrophage inhibitory protein-1beta; and regulated upon activation, normal T cell expressed and secreted in the livers of patients with FHF compared with those of LD. Macrophages and their expression of FasL may play roles in the pathogenesis of FHF. OBJECTIVES:The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement.METHODS:The subjects were 24 patients with FHF who underwent liver transplantation at our institution. For comparison, nine chronic hepatitis (CH) patients and six living liver donors (LD) were also enrolled. Liver tissues were obtained for histological (hematoxylin-eosin, terminal deoxynucleotidyl transferase [TdT]-mediated dUTP-biotin nick-end labeling [TUNEL], immunohistochemistry, and double immunofluorescence staining) and reverse transcription PCR (RT-PCR; cytokines and chemokines) analysis.RESULTS:The numbers of TUNEL-, FasL-, and CD68-positive cells in the livers of patients with FHF were significantly larger than in those with CH or with normal livers. Double immunofluorescence staining showed that FasL was expressed predominantly on liver macrophages and rarely on CD8-positive lymphocytes. RT-PCR study showed increased expression of FasL; interferon-γ; interleukin-18; macrophage inhibitory protein-1β; and regulated upon activation, normal T cell expressed and secreted in the livers of patients with FHF compared with those of LD.CONCLUSIONS:Macrophages and their expression of FasL may play roles in the pathogenesis of FHF. OBJECTIVES:The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical study was carried out to assess which cells expressed Fas-FasL and to determine their involvement. METHODS:The subjects were 24 patients with FHF who underwent liver transplantation at our institution. For comparison, nine chronic hepatitis (CH) patients and six living liver donors (LD) were also enrolled. Liver tissues were obtained for histological (hematoxylin-eosin, terminal deoxynucleotidyl transferase [TdT]-mediated dUTP-biotin nick-end labeling [TUNEL], immunohistochemistry, and double immunofluorescence staining) and reverse transcription PCR (RT-PCR; cytokines and chemokines) analysis. RESULTS:The numbers of TUNEL-, FasL-, and CD68-positive cells in the livers of patients with FHF were significantly larger than in those with CH or with normal livers. Double immunofluorescence staining showed that FasL was expressed predominantly on liver macrophages and rarely on CD8-positive lymphocytes. RT-PCR study showed increased expression of FasL; interferon-g; interleukin-18; macrophage inhibitory protein-1b; and regulated upon activation, normal T cell expressed and secreted in the livers of patients with FHF compared with those of LD. CONCLUSIONS:Macrophages and their expression of FasL may play roles in the pathogenesis of FHF.The American Journal of Gastroenterology (2005) 100, 2551-2559; doi:10.1111/j.1572-0241.2005.00265.x |
| Author | Kawakubo, Masatomo Miyagawa, Shin-ichi Tagawa, Yoh-ichi Nakayama, Jun Hashikura, Yasuhiko Mita, Atsuyoshi |
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| Keywords | Human Fas ligand Liver failure Gastroenterology Digestive diseases Hepatic disease Fulminant Macrophage |
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| Snippet | The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined. This clinical... OBJECTIVES:The mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined.... OBJECTIVESThe mechanisms of Fas-Fas ligand (Fas-FasL)-mediated apoptosis in the pathogenesis of fulminant hepatic failure (FHF) have not been well defined.... |
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| SubjectTerms | Adolescent Adult Antigens, CD - analysis Antigens, Differentiation, Myelomonocytic - analysis Antigens, Surface - analysis Apoptosis - immunology Biological and medical sciences Chemokine CCL4 Chemokine CCL5 - analysis Child Child, Preschool Fas Ligand Protein fas Receptor - analysis Female Gastroenterology Gastroenterology. Liver. Pancreas. Abdomen Hepatitis, Chronic - immunology Hepatitis, Chronic - pathology Humans Infant Interferon gamma Receptor Interferon-gamma - analysis Interleukin-18 - analysis Liver - immunology Liver - pathology Liver Failure, Acute - immunology Liver Failure, Acute - pathology Liver Transplantation Liver. Biliary tract. Portal circulation. Exocrine pancreas Living Donors Macrophage Inflammatory Proteins - analysis Macrophages - immunology Male Medical sciences Membrane Glycoproteins - analysis Other diseases. Semiology Receptors, Interferon - analysis Tumor Necrosis Factors - analysis |
| Title | Expression of Fas Ligand by Hepatic Macrophages in Patients with Fulminant Hepatic Failure |
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