AIM: To investigate the effect of Lactobacillus bulgaricus (LBG) on the Toll-like receptor 4 (TLR4) pathway and interleukin-8 (IL-8) production in SGC-7901 cells treated with Helicobacter pyloriSydney strain 1 lipopolysaccharide (H pyloriSS1-LPS). METHODS: SGC-7901 cells were treated with H pyloriSS1-LPS in the presence or absence of pretreatment for 1 h with viable LBG or supernatant recovered from LBG culture MRS broth (LBG-(s)). Cellular lysates were prepared for Western blot with anti-TLR4, anti-transforming growth factor beta-activated kinase 1 (TAK1), anti-phospho-TAK1, anti-nuclear factor kappaB (NF-kappaB), anti-p38 mitogen-activated protein kinase (p38MAPK), and anti-phospho-p38MAPK antibodies. The amount of IL-8 in cell culture medium was measured by ELISA. RESULTS: H pyloriSS1-LPS up-regulated the expression of TLR4, stimulated the phosphorylation of TAK1, subsequently enhanced the activation of NF-kappaB and the phosphorylation of p38MAPK in a time-dependent manner, leading to augmentation of IL-8 production in SGC-7901 cells. Viable LBG or LBG-(s) pretreatment attenuated the expression of TLR4, inhibited the phosphorylation of TAK1 and p38MAPK, prevented the activation of NF-kappaB, and consequently blocked IL-8 production. CONCLUSION: H pyloriSS1-LPS induces IL-8 production through activating TLR4 signaling in SGC-7901 cells and viable LBG or LBG-(s) prevents H pyloriSS1-LPS-mediated IL-8 production via inhibition of the TLR4 pathway.
AIM: To investigate the effect of Lactobacillus bulgaricus (LBG) on the Toll-like receptor 4 (TLR4) pathway and interleukin-8 (IL-8) production in SGC-7901 cells treated with Helicobacter pyloriSydney strain 1 lipopolysaccharide (H pyloriSS1-LPS). METHODS: SGC-7901 cells were treated with H pyloriSS1-LPS in the presence or absence of pretreatment for 1 h with viable LBG or supernatant recovered from LBG culture MRS broth (LBG-(s)). Cellular lysates were prepared for Western blot with anti-TLR4, anti-transforming growth factor beta-activated kinase 1 (TAK1), anti-phospho-TAK1, anti-nuclear factor kappaB (NF-kappaB), anti-p38 mitogen-activated protein kinase (p38MAPK), and anti-phospho-p38MAPK antibodies. The amount of IL-8 in cell culture medium was measured by ELISA. RESULTS: H pyloriSS1-LPS up-regulated the expression of TLR4, stimulated the phosphorylation of TAK1, subsequently enhanced the activation of NF-kappaB and the phosphorylation of p38MAPK in a time-dependent manner, leading to augmentation of IL-8 production in SGC-7901 cells. Viable LBG or LBG-(s) pretreatment attenuated the expression of TLR4, inhibited the phosphorylation of TAK1 and p38MAPK, prevented the activation of NF-kappaB, and consequently blocked IL-8 production. CONCLUSION: H pyloriSS1-LPS induces IL-8 production through activating TLR4 signaling in SGC-7901 cells and viable LBG or LBG-(s) prevents H pyloriSS1-LPS-mediated IL-8 production via inhibition of the TLR4 pathway.
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Authors: Katja Hattar; Christian P Reinert; Ulf Sibelius; Mira Y Gökyildirim; Florentine S B Subtil; Jochen Wilhelm; Bastian Eul; Gabriele Dahlem; Friedrich Grimminger; Werner Seeger; Ulrich Grandel Journal: Cancer Immunol Immunother Date: 2017-03-17 Impact factor: 6.968