Regulation of electrolyte transport with IL-1β in rabbit distal colon

Interletrkin-1β levels are elevated in inflammatory bowel disease. In this study the mechanism by which interleukin-1β affects electrolyte transport in the rabbit distal colon, was investigated. Interleukin-1β caused a delayed increase in short-circuit current (Isc) which was attributed to protein s...

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Bibliographic Details
Main Authors: F. R. Homaidan, H. Desai, L. Zhao, G. Broutman, R. Burakoff
Format: Article
Language:English
Published: Wiley 1995-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/S0962935195000111
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Summary:Interletrkin-1β levels are elevated in inflammatory bowel disease. In this study the mechanism by which interleukin-1β affects electrolyte transport in the rabbit distal colon, was investigated. Interleukin-1β caused a delayed increase in short-circuit current (Isc) which was attributed to protein synthesis since the effect was inhibited by cycloheximide. The interleukin-1β induced increase in Isc was not affected by amiloride treatment but was completely inhibited by bumetanide or in chloride-free buffer and by indomethacin. Prostaglandin E2 levels increased in tissue treated with interleukin-1β, but this increase was reversed by cycloheximide. These data suggest that interleukin-1β causes its effect via a yet to be identified second messenger, by increasing chloride secretion through a prostaglandin E2 mediated mechanism.
ISSN:0962-9351
1466-1861