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• W2047445859 abstract "Inflammatory bowel disease (IBD) is characterized by a dysregulated intestinal immune response with elevated levels of the Th1 cytokines TNF, IL-12 and IFN-γ. The luminal flora has been implicated as a major factor contributing to the initiation and perpetuation of chronic intestinal inflammation by as yet unknown mechanisms. Bacterial DNA contains unmethylated cytosine-guanosine dinucleotides (CpG) which strongly activate Th1-mediated immune responses. To test whether these CpG-motifs contribute to intestinal inflammation we treated mice with dextran-sulfate-sodium (DSS)-induced acute or chronic colitis for 5 days with CpG-containing oligodeoxynucleotides (CpG-ODN). Colonic inflammation was assessed by histological scoring. Colonic cytokine RNA was quantified by reverse transcription-PCR and cytokine secretion from mesenterial lymph node cells by ELISA. In chronic colitis, CpG-ODN treatment severely aggravated inflammation by 50%. Colonic expression of IFN-γ and TNF was elevated (200- and 150-fold, respectively) and IFN-γ and IL-12 secretion from lymph node cells was increased 5,000- and 8-fold, respectively, compared to GpG-ODN-treated controls. Similar effects were obtained in acute colitis. In conclusion, CpG-motifs of bacterial DNA have proinflammatory activity by strengthening the Th1 arm of immunity in DSS-induced colitis, and might therefore play asignificant role in the initiation and perpetuation of inflammation in IBD." @default.
• W2047445859 created "2016-06-24" @default.
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• W2047445859 date "2002-07-01" @default.
• W2047445859 modified "2023-10-14" @default.
• W2047445859 title "CpG motifs of bacterial DNA exacerbate colitis of dextran sulfate sodium-treated mice" @default.
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• W2047445859 doi "https://doi.org/10.1002/1521-4141(200207)32:7<2084::aid-immu2084>3.0.co;2-q" @default.
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