Interplay of IL-33 and IL-35 Modulates Th2/Th17 Responses in Cigarette Smoke Exposure HDM-Induced Asthma

Liu, Jing; Su, Beiting; Tao, Peizhi; Yang, Xuena; Zheng, Li; Lin, Yusen; Zou, Xiaoling; Yang, Hailing; Wu, Wenbin; Zhang, Tiantuo; Li, Hongtao

doi:10.1007/s10753-023-01902-6

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2024

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Cited by 2 publications

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Oxidative Stress-Based Toxicity of Chemical and Physical Agents

Khelfi,

Deffaf,

Hedhili

2024

Biomarkers of Oxidative Stress

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Oxidative Stress-Based Toxicity of Chemical and Physical Agents

Khelfi,

Deffaf,

Hedhili

2024

Biomarkers of Oxidative Stress

View full text Add to dashboard Cite

Nrf2 Deficiency Accelerates IL-17-Dependent Neutrophilic Airway Inflammation in Asthmatic Mice

Kuramoto,

Morishima,

Yoshida

et al. 2024

Antioxidants

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Asthma is a heterogeneous disease that can be broadly classified into type 2, which is primarily steroid-sensitive and eosinophilic, and non-type 2, which is primarily steroid-resistant and neutrophilic. While the mechanisms leading to the development of molecular-targeted therapies for type 2 asthma are being elucidated, much remains to be learned about non-type 2 asthma. To investigate the role of oxidative stress in refractory allergic airway inflammation, we compared asthma models generated by immunizing wild-type and nuclear factor erythroid-2-related factor 2 (Nrf2)-deficient mice with the house dust mite antigen. Both asthma models had similar levels of airway inflammation and hyperresponsiveness, but the Nrf2-deficient mice had increased oxidative stress and exacerbated neutrophilic airway inflammation compared with the wild-type mice. Type 2 cytokines and the expression of GATA3, a transcription factor that is important for Th2 cell differentiation, had decreased in Nrf2-deficient mice compared with the wild-type mice, whereas helper T (Th) 17 cytokines and the expression of RORγt, which is important for Th17 cell differentiation, had increased. Furthermore, the neutrophilic airway inflammation caused by Nrf2 deficiency was ameliorated by interleukin (IL)-17 neutralization. We have concluded that the disruption of the Nrf2-mediated antioxidant defense system contributed to the induction of Th17 differentiation and exacerbated allergic neutrophilic airway inflammation.

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Interplay of IL-33 and IL-35 Modulates Th2/Th17 Responses in Cigarette Smoke Exposure HDM-Induced Asthma

Cited by 2 publications

References 69 publications

Oxidative Stress-Based Toxicity of Chemical and Physical Agents

Oxidative Stress-Based Toxicity of Chemical and Physical Agents

Nrf2 Deficiency Accelerates IL-17-Dependent Neutrophilic Airway Inflammation in Asthmatic Mice

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