Brief Reports
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 1, 2004; 10(3): 455-457
Published online Feb 1, 2004. doi: 10.3748/wjg.v10.i3.455
Probiotics inhibit TNF-α-induced interleukin-8 secretion of HT29 cells
Ai-Ping Bai, Qin Ouyang, Wen Zhang, Chun-Hui Wang, Sheng-Fu Li
Ai-Ping Bai, Qin Ouyang, Chun-Hui Wang, Department of Gastroenterology, Huaxi Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
Wen Zhang, Department of Hepatology, First Hospital of Xiangfan City, Xiangfan 441000, Hubei Province, China
Sheng-Fu Li, Institute of Transplantation and Immunology, Huaxi Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
Correspondence to: Ai-Ping Bai, Department of Gastroenterology, Huaxi Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China. baiap@163.com
Telephone: +86-28-85422386
Received: June 5, 2003
Revised: July 4, 2003
Accepted: July 30, 2003
Published online: February 1, 2004
Abstract

AIM: To study the effect of probiotics on interleukin-8 secretion in intestinal epithelia when stimulated by proinflammatory cytokines.

METHODS: Colonic adenocarcinoma HT29 cells were cultured and divided into four groups: control, TNF-α (group T in short), bifidobacterium (group B), lactobacillus (group L). B. Longum and L. bulgaricus were suspended in culture medium with a concentration of 1 × 108 cfu/ml and added into 24 wells respectively. One hour later TNF-α (10 ng/ml) was added into each well of groups T, B, L. The supernatants were collected and measured for IL-8 after 3 hours, nuclear factor-kB (NF-κB) p65 was also examined by Western blotting.

RESULTS: There was less interleukin-8 secretion in HT29 cells when preincubated with B. Longum or L. bulgaricus compared with group T. Less p65 appeared in nuclei in groups B and L compared with group T, as detected by Western blot.

CONCLUSION: Probiotics can suppress interleukin-8 secretion in intestinal epithelia when stimulated by proinflammatory cytokines, which is most likely mediated by NF-κB.

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