title: Differences in TLR9-dependent inhibitory effects of H(2)O(2)-induced IL-8 secretion and NF-kappa B/I kappa B-alpha system activation by genomic DNA from five Lactobacillus species.
abstract: Lactic acid bacteria (LAB) show anti-inflammatory effects, and their genomic DNA was identified as one of the anti-inflammatory components. Despite the differences in anti-inflammatory effects between live LAB dependent not only on genus but also species, this effect has not been compared at the genomic DNA level. We compared the anti-inflammatory effects of the genomic DNA from five Lactobacillus species-Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus gasseri, Lactobacillus plantarum, and Lactobacillus reuteri-using Caco-2 cells. To evaluate anti-inflammatory effects, decreases in H(2)O(2)-induced IL-8 secretion and inhibition of H(2)O(2)-induced NF-κB/IκB-α system activation were examined. All LAB genomic DNAs dose-dependently decreased H(2)O(2)-induced IL-8 secretion and inhibited H(2)O(2)-induced NF-κB/IκB-α system activation. Comparison of these effects between Lactobacillus species showed that the anti-inflammatory effects of L. acidophilus genomic DNA are lower than those of the other species. Furthermore, suppression of Toll-like receptor 9 (TLR9), a specific receptor of bacterial DNA, expression by RNAi abolished the decrease of H(2)O(2)-induced IL-8 secretion and inhibition of H(2)O(2)-induced NF-κB/IκB-α system activation by LAB genomic DNA. Our results demonstrated that the anti-inflammatory effects of genomic DNA differ between Lactobacillus species and TLR9 is one of the major pathways responsible for the anti-inflammatory effect of LAB genomic DNA.
authors.affiliation: Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan.
authors.forename: Yukihiro
authors.initials: Y
authors.lastname: Hiramatsu
authors.forename: Tomomitsu
authors.initials: T
authors.lastname: Satho
authors.forename: Keiichi
authors.initials: K
authors.lastname: Irie
authors.forename: Shota
authors.initials: S
authors.lastname: Shiimura
authors.forename: Takahiro
authors.initials: T
authors.lastname: Okuno
authors.forename: Tanjina
authors.initials: T
authors.lastname: Sharmin
authors.forename: Saori
authors.initials: S
authors.lastname: Uyeda
authors.forename: Yuki
authors.initials: Y
authors.lastname: Fukumitsu
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Nakashima
authors.forename: Fumio
authors.initials: F
authors.lastname: Miake
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Kashige
mesh_terms: D021581:Active Transport, Cell Nucleus; D000893:Anti-Inflammatory Agents / Q000276:immunology; D018938:Caco-2 Cells; D002467:Cell Nucleus / Q000187:drug effects / Q000473:pathology; D004269:DNA, Bacterial / Q000235:genetics / Q000276:immunology*; D004305:Dose-Response Relationship, Drug; D004926:Escherichia coli / Q000235:genetics / Q000276:immunology; D016680:Genome, Bacterial; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D020672:I-kappa B Proteins / Q000276:immunology / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism*; D007778:Lactobacillus / Q000235:genetics* / Q000276:immunology; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000276:immunology / Q000378:metabolism; D059748:Proteolysis; D034622:RNA Interference; D015398:Signal Transduction; D051217:Toll-Like Receptor 9 / Q000276:immunology* / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; C508606:CXCL8 protein, human; D004269:DNA, Bacterial; D020672:I-kappa B Proteins; D016209:Interleukin-8; D016328:NF-kappa B; C000606204:NFKBIA protein, human; C495371:TLR9 protein, human; D051217:Toll-Like Receptor 9; D000072000:NF-KappaB Inhibitor alpha; D006861:Hydrogen Peroxide