Abstract
BackgroundInterleukin (IL)-8 is the key agent for initiating an inflammatory response to infection with Helicobacter pylori. Some strains of Lactobacillus spp. are known to colonize the stomach and suppress inflammation caused by H. pylori. In this study, we characterized two gastric-derived lactobacilli, Lactobacillus salivarius (LS) strains B37 and B60, capable of inhibiting H. pylori-induced IL-8 production by gastric epithelial cells.ResultsConditioned media from LS-B37 and LS-B60 suppressed H. pylori-induced IL-8 production and mRNA expression from AGS cells without inhibiting H. pylori growth. These conditioned media suppressed the activation of NF-κB but did not suppress c-Jun activation. IL-8 inhibitory substances in conditioned media of LS-B37 and LS-B60 are heat-stable and larger than 100 kDa in size. The inhibitory activity of LS-B37 was abolished when the conditioned medium was treated with α-amylase but still remained when treated with either proteinase K, trypsin, lipase or lysozyme. The activity of LS-B60 was abolished when the conditioned medium was treated with either amylase or proteinase K but still remained when treated with lysozyme. Treatment with lipase and trypsin also significantly affected the inhibitory activity of LS-B60 although the conditioned medium retained IL-8 suppression statistically different from media control.ConclusionsThese results suggest that L. salivarius strains B37 and B60 produce different immunomodulatory factors capable of suppressing H. pylori-induced IL-8 production from gastric epithelial cells. Our results suggest that the large, heat-stable immunomodulatory substance(s) present in the LCM of LS-B37 is a polysaccharide, while the one(s) of LS-B60 is either complex consisting of components of polysaccharide, lipid and protein or includes multiple components such as glycoprotein and lipoprotein.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-016-0861-x) contains supplementary material, which is available to authorized users.
Highlights
Interleukin (IL)-8 is the key agent for initiating an inflammatory response to infection with Helicobacter pylori
H. pylori infection induces the production of pro-inflammatory cytokines and chemokines such as interleukin (IL)-1β, IL-6, IL-8, IL-23 and tumor necrosis factor (TNF)-α [3,4,5] resulting in gastric inflammation characterized by the infiltration
We hypothesized that L. salivarius B37 and B60 may suppress IL-8 gene expression at other time points or affect IL-8 production posttranscriptionally or post-translationally. The results of this present study demonstrated that L. salivarius B37 and L. salivarius B60 produce distinct active components that inhibit Nuclear factor-kappa B (NF-κB) activation and suppress downstream transcription of H. pylori-induced IL-8 mRNA
Summary
Interleukin (IL)-8 is the key agent for initiating an inflammatory response to infection with Helicobacter pylori. We characterized two gastric-derived lactobacilli, Lactobacillus salivarius (LS) strains B37 and B60, capable of inhibiting H. pylori-induced IL-8 production by gastric epithelial cells. H. pylori infection induces the production of pro-inflammatory cytokines and chemokines such as interleukin (IL)-1β, IL-6, IL-8, IL-23 and tumor necrosis factor (TNF)-α [3,4,5] resulting in gastric inflammation characterized by the infiltration. We previously reported eight isolates of Lactobacillus spp. which inhibited IL-8 secretion from H. pylori-infected AGS cells [26]. Among these lactobacilli, L. salivarius B101, L. rhamnosus B103 and L. plantarum XB7 suppressed IL-8 mRNA expression and the activation of NF-κB whereas L. plantarum XB7 suppressed c-Jun activation. L. salivarius B37, L. salivarius B60 and the other three strains inhibited the secretion of IL-8 but did not interfere with IL-8 gene transcription after co-culture for 4 h with AGS cells
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