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Войти в исследования Annals of clinical and laboratory science · 2026
Indoleamine 2,3-dioxygenase Suppresses Neutrophilic Airway Inflammation by Regulating Th17 and Treg Responses.
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Chen Zhiqiang, Hu Ying, Zeng Jing, Cai Na, Zheng Shouyan, Liao Wei
Аннотация
OBJECTIVE: Th17 cells play an important role in the promotion of asthma inflammation. Indoleamine 2,3-dioxygenase (IDO)-dependent tryptophan metabolism has been shown to act as a molecular "switch" for the conversion of Th17 cells into Tregs under certain conditions.
METHODS: A neutrophilic asthma model was established using ovalbumin (OVA) and lipopolysaccharide. IDO expression in the model mice was regulated using an IDO inducer and an IDO inhibitor. Th17 cells and the secretion of related factors were examined, and changes in airway hyperreactivity and inflammation were observed. Plasmacytoid dendritic cells and naïve CD4+ T cells were co-cultured in vitro. After OVA stimulation and IDO inhibitor treatment, changes in Th17 cells and the secretion of related factors were examined.
RESULTS: Airway hyperreactivity and inflammation were ameliorated in the neutrophilic asthma model mice in the IDO inducer group. Compared to the asthma model group, the IDO inducer group showed decreased Th17 cell percentages, increased Treg cell percentages in the peripheral blood, and reduced levels of IL-17, IL-6, and TGF-β1 in the BALF and lung tissues; IDO inhibited RORγt expression and promoted Foxp3 expression in the neutrophilic asthma model. Moreover, IDO inhibited DC-mediated Th17 cell differentiation and secretion of related cytokines, whereas these effects were reversed by the IDO inhibitor.
CONCLUSION: IDO ameliorated airway hyperreactivity and inflammation in neutrophilic asthma by inhibiting Th17 cells and inducing Treg production. These results will provide a new basis for developing potential therapeutic targets for the prevention and treatment of neutrophilic asthma using IDO.
METHODS: A neutrophilic asthma model was established using ovalbumin (OVA) and lipopolysaccharide. IDO expression in the model mice was regulated using an IDO inducer and an IDO inhibitor. Th17 cells and the secretion of related factors were examined, and changes in airway hyperreactivity and inflammation were observed. Plasmacytoid dendritic cells and naïve CD4+ T cells were co-cultured in vitro. After OVA stimulation and IDO inhibitor treatment, changes in Th17 cells and the secretion of related factors were examined.
RESULTS: Airway hyperreactivity and inflammation were ameliorated in the neutrophilic asthma model mice in the IDO inducer group. Compared to the asthma model group, the IDO inducer group showed decreased Th17 cell percentages, increased Treg cell percentages in the peripheral blood, and reduced levels of IL-17, IL-6, and TGF-β1 in the BALF and lung tissues; IDO inhibited RORγt expression and promoted Foxp3 expression in the neutrophilic asthma model. Moreover, IDO inhibited DC-mediated Th17 cell differentiation and secretion of related cytokines, whereas these effects were reversed by the IDO inhibitor.
CONCLUSION: IDO ameliorated airway hyperreactivity and inflammation in neutrophilic asthma by inhibiting Th17 cells and inducing Treg production. These results will provide a new basis for developing potential therapeutic targets for the prevention and treatment of neutrophilic asthma using IDO.