Detailed Abstract
[E-poster]
[EP124] Serum level of visfatin can predict the severity of inflammation in patients with acute cholecystitis
Jae Woo PARK1, Tae Ho HONG3, Ho Joong CHOI3, Jung Hyun PARK5, Kee-Hwan KIM6, Dong Do YOU4, Jae Hyun HAN4, Kwang Yeol PAIK2, Say-June KIM*3
1Department of Surgery, Daejeon St. Mary's Hospital, College of Medicine, the Catholic University of Korea, Seoul, Republic of Korea, Korea
2Department of Surgery, Yeouido ST. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Korea
3Department of Surgery, Seoul St. Mary’s Hospital, College of Medicine, the Catholic University of Korea, Korea
4Department of Surgery, St. Paul's Hospital, College of Medicine, the Catholic University of Korea, Korea
5Department of Surgery, Eunpeong St. Mary's Hospital, College of Medicine, the Catholic University of Korea, Korea
6Department of Surgery, Uijeongbu St. Mary's Hospital, College of Medicine, the Catholic University of Korea, Korea
Introduction : Visfatin is a key cytokine released from the peripheral blood mononuclear cells (PBMCs) as well as adipose tissue, and it is involved in immune response as well as inflammation. In this study, we investigated whether the serum visfatin level could be a prognostic factor for predicting the severity of inflammation in patients with acute cholecystitis.
Methods : We examined the blood samples and gallbladder specimens from patients who underwent laparoscopic cholecystectomy for either acute (N = 18) or chronic cholecystitis (N = 18). We determined the visfatin levels of these samples using various procedures such as real-time PCR, ELISA, western blotting, and immunohistochemistry.
Results : The patients with acute cholecystitis exhibited higher mRNA expression of visfatin in PBMCs, higher serum levels of visfatin, and increased protein expression of visfatin in the gallbladder specimens than in patients with chronic cholecystitis. In the in vitro model of acute cholecystitis, the mRNA expression of visfatin showed the fastest increase among the other pro-inflammatory mediators studied, including IL-10, TNF-α, IL-6, ICAM-1, and VCAM-1. Inhibition of visfatin using si-RNA abrogated the inhibitory effects of LPS on the expression of ABCG1 in GBECs, suggesting that visfatin is significantly involved in the LPS-driven suppression of ABCG1.
Conclusions : Taken together, we concluded that visfatin is a pro-inflammatory mediators that is upregulated during acute cholecystectomy and is expected to be increased within a short time after inflammation. Therefore, measuring the serum level of visfatin would be helpful in predicting the inflammatory severity in the patients with acute cholecystitis.
Methods : We examined the blood samples and gallbladder specimens from patients who underwent laparoscopic cholecystectomy for either acute (N = 18) or chronic cholecystitis (N = 18). We determined the visfatin levels of these samples using various procedures such as real-time PCR, ELISA, western blotting, and immunohistochemistry.
Results : The patients with acute cholecystitis exhibited higher mRNA expression of visfatin in PBMCs, higher serum levels of visfatin, and increased protein expression of visfatin in the gallbladder specimens than in patients with chronic cholecystitis. In the in vitro model of acute cholecystitis, the mRNA expression of visfatin showed the fastest increase among the other pro-inflammatory mediators studied, including IL-10, TNF-α, IL-6, ICAM-1, and VCAM-1. Inhibition of visfatin using si-RNA abrogated the inhibitory effects of LPS on the expression of ABCG1 in GBECs, suggesting that visfatin is significantly involved in the LPS-driven suppression of ABCG1.
Conclusions : Taken together, we concluded that visfatin is a pro-inflammatory mediators that is upregulated during acute cholecystectomy and is expected to be increased within a short time after inflammation. Therefore, measuring the serum level of visfatin would be helpful in predicting the inflammatory severity in the patients with acute cholecystitis.
SESSION
E-poster
E-Session 7/27 ~ 7/29 ALL DAY