Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0603820130190020158
Journal of Experimental & Biomedical Science
2013 Volume.19 No. 2 p.158 ~ p.163
Interleukin-2 Inhibits Secretin-Induced Bile Secretion in Cholangiocytes
Ko Yoo-Seung

Hwang Seock-Yeon
Park Jae-Seung
Abstract
Cholestatic liver is associated with hepatic inflammation and elevated proinflammatory cytokines. Recent studies indicate that certain cytokines can modulate bile secretion. In the present study, we have examined the role of interleukin (IL-2) on the bile secretion by a combination of study models. To examine the relevance of IL-2 on bile secretion, the expression of IL-2 and IL-2 receptor (IL-2R) of isolated normal and bile duct ligated (BDL) rats cholangiocytes was first measured by RT-PCR. In BDL rats, the expression of IL-2 and IL-2R was significantly increased compared with normal rats. To study the effect of IL-2 on bile secretion, bile flow was measured in normal and BDL rats. At the level of cholangiocytes, secretory responses of isolated bile duct unit (IBDU)s were quantified by videomicroscopy. The administrations of IL-2 had no significant effect on basal bile secretion in normal and BDL rats. There was no significant effect of IL-2 on basal bile ductular secretion as evidenced by no significant difference in luminal area of the IBDUs perfusedwith 100 pM of IL-2 from those of albumin carrier control. However, the secretin-stimulated bile ductular secretion was significantly (P £¼ 0.01) inhibited by 34 ¡¾ 4% (normal, n = 12), 21 ¡¾ 5.3% (BDL 2 wk, n = 12) and 15 ¡¾ 5.2% (BDL 4 wk, n = 12) with the co-administration of IL-2. As with other cytokines, physiologically relevant concentration of IL-2 can significantly inhibit secretin-stimulated bile ductular secretion. These findings support the important roles of cytokines in modulating bile secretion and may contribute to the cholestasis seen in cholestatic liver diseases.
KEYWORD
Interleukin-2, Secretin, Cholangiocytes, Bile secretion, Cholestatic liver, Bile duct ligation (BDL)
FullTexts / Linksout information
Listed journal information
ÇмúÁøÈïÀç´Ü(KCI)