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How do Lactobacilli treat Helicobacter pylori-related diseases?
Date:9/9/2008

Some studies have demonstrated H. pylori stimulates the release of interleukin-8 (IL-8) from gastric epithelia, which initiates inflammatory damage to gastric mucosa and plays a crucial role in the pathogenesis of H. pylori infections. H. pylori lipopolysaccharide (H. pylori-LPS) is the major initiator in H. pylori-induced IL-8 production via activation of Toll-like receptor 4 (TLR4) pathway in gastric epithelia. Considering the novel finding that H. pylori is an indigenous biota in gastric microflora including Lactobacilli and hypothesis that the disturbance of gastric microecosystem plays a more important role in pathogenetic mechanisms of H. pylori, the eradiation of H. pylori doesn't seem justified to everyone. The speculation on validity of restoration of the gastric microecosystem has been demonstrated by therapeutic effects of Lactobacilli administration on H. pylori-associated diseases. But whether Lactobacilli inhibit H. pylori-LPS-induced IL-8 production through blocking H. pylori-LPS-activated TLR4 pathway hasn't been well researched.

A research article to be published on August 28, 2008 in the World Journal of Gastroenterology addresses this question. The research team led by Prof. Hong-Sheng Ma from West China Hospital of Sichuan University treated SGC-7901 cells with H. pylori Sydney strain 1 lipopolysaccharide (H. pyloriSS1-LPS) in the absence or presence of a pretreatment with viable Lactobacillus bulgaricus (LBG). The results indicated that viable LBG prevented H. pyloriSS1-LPS-activated TLR4 pathway in SGC-7901 cells, leading to its inhibitory effect on IL-8 production stimulated by H. pyloriSS1-LPS. Considering some evidence implied that supernatant recovered from Lactobacilli culture MRS broth contained some latent soluble proteins secreted by Lactobacilli, SGC-7901 cells were treated wi
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Contact: Lai-Fu Li
wjg@wjgnet.com
86-105-908-0039
World Journal of Gastroenterology
Source:Eurekalert

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