Modulation of airway inflammation by CpG oligodeoxynucleotides in a murine model of asthma.
Modulation of airway inflammation by CpG oligodeoxynucleotides in a murine model of asthma.
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发表时间:
1998
影响因子:
4.4
通讯作者:
J. Kline;T. Waldschmidt;T. Businga;J. E. Lemish;J. Weinstock;P. Thorne;A. Krieg
中科院分区:
文献类型:
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作者:
J. Kline;T. Waldschmidt;T. Businga;J. E. Lemish;J. Weinstock;P. Thorne;A. Krieg
Asthma has been increasing in industrialized countries. Evidence suggests that asthma is caused by a Th2 immune response to inhaled environmental Ags and that childhood infections protect against this. We have shown that bacterial DNA contains motifs, centered on unmethylated CpG dinucleotides, which induce Th1-type responses. We hypothesized that the Th1 effect of these CpG motifs may oppose the Th2 type allergic response and suggest that this may account for the protective effect of childhood infection against asthma. We examined the effects of CpG-motif oligodeoxynucleotides (CpG ODN) in a murine model of asthma. Airway eosinophilia, Th2 cytokine induction, IgE production, and bronchial hyperreactivity were prevented by coadministration of CpG ODN with the Ag. Significantly, in a previously sensitized mouse, CpG ODN can prevent allergen-induced airway inflammation. These studies suggest that exposure to CpG DNA may protect against asthma.