PMID- 10798742
OWN - NLM
STAT- MEDLINE
DCOM- 20000525
LR  - 20190713
IS  - 0041-1337 (Print)
IS  - 0041-1337 (Linking)
VI  - 69
IP  - 7
DP  - 2000 Apr 15
TI  - The protective role of Kupffer cells in humoral injury of xenoperfused rat 
      livers.
PG  - 1283-9
AB  - BACKGROUND: The role of Kupffer cells in a hepatic xenograft rejection is still 
      unclear. We investigated the effect of blocking Kupffer cells on xenogeneic 
      humoral injury using rat livers as the xenoperfusion models. METHODS: Rat livers 
      were perfused with fresh human blood after pretreatment either with normal saline 
      (group 1; n = 8) or with gadolinium chloride (GdCl3) solution (group 2; n = 8). 
      Tissue injury was evaluated by alanine aminotransferase release and histological 
      examination. Tumor necrosis factor-alpha (TNF-alpha) production from rat livers 
      was measured by enzyme-linked immunosorbent assay and also examined by 
      immunohistochemistry. In addition, Kupffer cells were isolated after pretreatment 
      either with normal saline or with GdCl3 solution and incubated with human serum. 
      Localization of human C3 and IgM was examined by immunofluorescence. RESULTS: 
      Alanine aminotransferase release in group 2 was significantly higher than in 
      group 1 (P = 0.015). Histological examination revealed more severe tissue injury 
      in group 2. The mean TNF-alpha level was not significantly different between the 
      two groups. In immunohistochemistry, TNF-alpha was positive primarily on vascular 
      endothelial cells in both groups. Immunofluorescence of saline-treated Kupffer 
      cells showed an uptake of human C3 in the cytoplasm, whereas no uptake was 
      observed in GdCl3-treated cells. The uptake of human IgM did not differ between 
      the two groups. CONCLUSIONS: These results suggest that Kupffer cells have a 
      protective role in preventing xenogeneic humoral injury. Their ability to absorb 
      xenogeneic complements may contribute to this protective mechanism.
FAU - Takeyama, O
AU  - Takeyama O
AD  - Department of Gastroenterological Surgery, Kyoto University Graduate School of 
      Medicine, Japan.
FAU - Ikai, I
AU  - Ikai I
FAU - Yamamoto, M
AU  - Yamamoto M
FAU - Kanazawa, A
AU  - Kanazawa A
FAU - Yagi, T
AU  - Yagi T
FAU - Uesugi, T
AU  - Uesugi T
FAU - Nishitai, R
AU  - Nishitai R
FAU - Satoh, S
AU  - Satoh S
FAU - Terajima, H
AU  - Terajima H
FAU - Yamaoka, Y
AU  - Yamaoka Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Transplantation
JT  - Transplantation
JID - 0132144
RN  - 0 (Antigens, Heterophile)
RN  - 0 (Complement C3)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - AU0V1LM3JT (Gadolinium)
RN  - EC 2.6.1.2 (Alanine Transaminase)
RN  - P7082WY76D (gadolinium chloride)
SB  - IM
CIN - Transplantation. 2002 Feb 15;73(3):483-4. PMID: 11884951
MH  - Alanine Transaminase/metabolism
MH  - Animals
MH  - Antigens, Heterophile/*physiology
MH  - *Blood Physiological Phenomena
MH  - Cells, Cultured
MH  - Complement C3/metabolism
MH  - Cytoplasm/metabolism
MH  - Fluorescent Antibody Technique
MH  - Gadolinium/pharmacology
MH  - Humans
MH  - Immunohistochemistry
MH  - Kupffer Cells/drug effects/metabolism/*physiology
MH  - Liver/pathology
MH  - *Liver Circulation
MH  - Male
MH  - Rats
MH  - Rats, Wistar
MH  - Tumor Necrosis Factor-alpha/metabolism/physiology
EDAT- 2000/05/08 09:00
MHDA- 2000/06/08 09:00
CRDT- 2000/05/08 09:00
PHST- 2000/05/08 09:00 [pubmed]
PHST- 2000/06/08 09:00 [medline]
PHST- 2000/05/08 09:00 [entrez]
AID - 10.1097/00007890-200004150-00013 [doi]
PST - ppublish
SO  - Transplantation. 2000 Apr 15;69(7):1283-9. doi: 10.1097/00007890-200004150-00013.