AJP - GI AJP: Renal Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Gastrointest Liver Physiol 280: G738-G745, 2001;
0193-1857/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McGill, J. M.
Right arrow Articles by Stansfield, A. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McGill, J. M.
Right arrow Articles by Stansfield, A. P.
Vol. 280, Issue 4, G738-G745, April 2001

Interleukin-5 inhibition of biliary cell chloride currents and bile flow

James M. McGill1,2, Margaret S. Yen2, Oscar W. Cummings3, Gianfranco Alpini5,6, Gene LeSage5, Karen E. Pollok4, Barbara Miller1, Steven K. Engle2, and Ann P. Stansfield2

1 Roudebush Veterans Affairs Medical Center and 2 Departments of Medicine and 3 Pathology, 4 Pediatric Hematology/Oncology, Herman B. Wells Center for Pediatric Research, Riley Hospital for Children; Indiana University School of Medicine, Indianapolis, Indiana 46202; and 5 Scott and White Hospital and The Texas Health Science Center College of Medicine and 6 Central Texas Veterans Health Care System, Temple, Texas 76502

Recent studies have detected significant elevations of interleukin (IL)-5 mRNA in the liver parenchyma of patients with both primary biliary cirrhosis and acute rejection after liver transplantation. In both of these disorders, intrahepatic biliary epithelial cells (BECs) are the targets of injury. We hypothesized that BECs may themselves express IL-5 receptors that may modulate key biliary functions. RNAs coding for IL-5alpha and -beta receptors were amplified by RT/PCR from a biliary cell line derived from a human cholangiocarcinoma (Mz-ChA-1) and verified by DNA sequencing. IL-5 receptor distribution was detected immunocytochemically on Mz-ChA-1 cells, immortalized murine BEC, bile duct-ligated rat liver, and isolated cholangiocytes. Patch-clamp studies on Mz-ChA-1 cells showed that IL-5 inhibits 5'-N-ethylcarboxamidoadenosine-stimulated chloride currents. Additional functional studies showed that IL-5 inhibits secretin-induced bile flow. We conclude that BECs express IL-5 receptors and that IL-5 modulates BEC chloride currents and fluid secretion. Since IL-5 has previously been associated with cholestatic liver disease, we speculate that IL-5 may contribute to liver injury through its effects on biliary secretion.

cholestatic liver disease; chloride channel; patch-clamp recording


This article has been cited by other articles:


Home page
J. Physiol.Home page
H. Sakai, Y. Ohira, A. Tanaka, T. Suzuki, A. Ikari, M. Morii, and N. Takeguchi
Inhibition of small-conductance Cl- channels by the interleukin-1{beta}-stimulated production of superoxide in rabbit gastric parietal cells
J. Physiol., August 15, 2003; 551(1): 207 - 217.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
N. Kanno, G. LeSage, S. Glaser, and G. Alpini
Regulation of cholangiocyte bicarbonate secretion
Am J Physiol Gastrointest Liver Physiol, September 1, 2001; 281(3): G612 - G625.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online