PMID- 9220535
OWN - NLM
STAT- MEDLINE
DCOM- 19970904
LR  - 20181130
IS  - 1081-650X (Print)
IS  - 1081-650X (Linking)
VI  - 109
IP  - 4
DP  - 1997 Jul
TI  - Promotion of leukocyte transendothelial cell migration by chemokines derived from 
      human biliary epithelial cells in vitro.
PG  - 372-82
AB  - Biliary epithelial cells are the focus of inflammatory damage in several liver 
      diseases, including allograft rejection wherein intrahepatic bile ducts are 
      infiltrated and damaged by T cells and neutrophils. Locally secreted chemotactic 
      cytokines (chemokines) are important signals for leukocyte recruitment to an 
      inflammatory site and include interleukin-8 (IL-8) and monocyte chemotactic 
      protein-1 (MCP-1), potent chemotactic agents for neutrophils and monocyte or T 
      cells, respectively. In this study, we demonstrate that primary cultures of human 
      biliary epithelial cells (BECs) express and secrete IL-8 and MCP-1, both of which 
      are upregulated rapidly and markedly in response to the proinflammatory cytokines 
      IL-1 and tumor necrosis factor-alpha. Interferon-gamma had a differential effect 
      by reducing IL-8 secretion but stimulating MCP-1 secretion. BECs cocultured in 
      transwell chambers below confluent monolayers of endothelial cells promoted the 
      transendothelial migration of neutrophils, which was blocked by antibodies to 
      CD18 or CD11b but only partially inhibited by blocking antibodies to IL-8. We 
      conclude that human BECs produce and secrete potent, functional chemokines when 
      stimulated by proinflammatory cytokines. The ability of BECs to secrete 
      chemokines and thus to promote leukocyte infiltration into portal tracts seems 
      likely to be an important cause of bile duct damage in such conditions as liver 
      allograft rejection and may explain the involvement of intrahepatic bile ducts in 
      a number of inflammatory liver diseases.
FAU - Morland, C M
AU  - Morland CM
AD  - Liver Research Laboratories, Queen Elizabeth Hospital, Edgbaston, Birmingham, 
      U.K.
FAU - Fear, J
AU  - Fear J
FAU - McNab, G
AU  - McNab G
FAU - Joplin, R
AU  - Joplin R
FAU - Adams, D H
AU  - Adams DH
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Proc Assoc Am Physicians
JT  - Proceedings of the Association of American Physicians
JID - 9514310
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Base Sequence
MH  - Biliary Tract/*cytology
MH  - Cells, Cultured
MH  - Chemokine CCL2/analysis/*metabolism
MH  - Chemotaxis, Leukocyte/drug effects/*physiology
MH  - Endothelium, Vascular/cytology/*physiology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Interleukin-1/administration & dosage/*physiology
MH  - Interleukin-8/analysis/*metabolism
MH  - Liver/blood supply
MH  - Molecular Sequence Data
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/analysis
MH  - Reference Values
MH  - Tumor Necrosis Factor-alpha/administration & dosage/*physiology
EDAT- 1997/07/01 00:00
MHDA- 1997/07/01 00:01
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/07/01 00:01 [medline]
PHST- 1997/07/01 00:00 [entrez]
PST - ppublish
SO  - Proc Assoc Am Physicians. 1997 Jul;109(4):372-82.