Division of Gastroenterology and Nutrition Winthrop-University Hospital Mineola NY 11501 USA.
Mediators Inflamm. 1995;4(1):61-6. doi: 10.1155/S0962935195000111.
Interletrkin-1beta levels are elevated in inflammatory bowel disease. In this study the mechanism by which interleukin-1beta affects electrolyte transport in the rabbit distal colon, was investigated. Interleukin-1beta caused a delayed increase in short-circuit current (I(sc)) which was attributed to protein synthesis since the effect was inhibited by cycloheximide. The interleukin-1beta induced increase in I(sc) was not affected by amiloride treatment but was completely inhibited by bumetanide or in chloride-free buffer and by indomethacin. Prostaglandin E(2) levels increased in tissue treated with interleukin-1beta, but this increase was reversed by cycloheximide. These data suggest that interleukin-1beta causes its effect via a yet to be identified second messenger, by increasing chloride secretion through a prostaglandin E(2) mediated mechanism.
白细胞介素-1β在炎症性肠病中升高。在这项研究中,研究了白细胞介素-1β如何影响兔远端结肠的电解质转运。白细胞介素-1β导致短路电流(Isc)延迟增加,这归因于蛋白质合成,因为该作用被环己酰亚胺抑制。白细胞介素-1β诱导的 Isc 增加不受阿米洛利处理的影响,但被布美他尼或无氯缓冲液和吲哚美辛完全抑制。白细胞介素-1β处理的组织中前列腺素 E2(PGE2)水平增加,但该增加被环己酰亚胺逆转。这些数据表明,白细胞介素-1β通过尚未确定的第二信使通过增加通过前列腺素 E2 介导的机制的氯分泌来发挥其作用。