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-alpha (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 x 10(8) cfu/ml and added into 24 wells respectively. One hour later TNF-alpha (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-kappaB (NF-kappaB) 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-kappaB.
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-alpha (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 x 10(8) cfu/ml and added into 24 wells respectively. One hour later TNF-alpha (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-kappaB (NF-kappaB) 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-kappaB.
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