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Microbes Infect ; 15(2): 96-104, 2013 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23182970

RESUMO

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.


Assuntos
DNA Bacteriano/imunologia , Peróxido de Hidrogênio/farmacologia , Interleucina-8/metabolismo , Lactobacillus/genética , Receptor Toll-Like 9/imunologia , Transporte Ativo do Núcleo Celular , Anti-Inflamatórios/imunologia , Células CACO-2 , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/patologia , DNA Bacteriano/genética , Relação Dose-Resposta a Droga , Escherichia coli/genética , Escherichia coli/imunologia , Genoma Bacteriano , Humanos , Proteínas I-kappa B/imunologia , Proteínas I-kappa B/metabolismo , Lactobacillus/imunologia , Inibidor de NF-kappaB alfa , NF-kappa B/imunologia , NF-kappa B/metabolismo , Proteólise , Interferência de RNA , Transdução de Sinais , Receptor Toll-Like 9/metabolismo
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