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Macrophage-intrinsic DUOX1 contributes to type 2 inflammation and mucus metaplasia during allergic airway disease. | LitMetric

AI Article Synopsis

  • The NADPH oxidase DUOX1 is essential for producing alarmins like IL-33 in response to allergens, contributing to mucus production and airway changes in chronic allergic diseases.
  • Researchers deleted DUOX1 from lung epithelial cells and macrophages to investigate its specific roles during both acute and chronic responses to house dust mite allergens.
  • The study found that DUOX1 in epithelial cells drives acute airway responses, while its presence in macrophages is crucial for type 2 cytokine production and macrophage activity during chronic inflammation.

Article Abstract

The NADPH oxidase DUOX1 contributes to epithelial production of alarmins, including interleukin (IL)-33, in response to injurious triggers such as airborne protease allergens, and mediates development of mucus metaplasia and airway remodeling in chronic allergic airways diseases. DUOX1 is also expressed in non-epithelial lung cell types, including macrophages that play an important role in airway remodeling during chronic lung disease. We therefore conditionally deleted DUOX1 in either lung epithelial or monocyte/macrophage lineages to address its cell-specific actions in innate airway responses to acute airway challenge with house dust mite (HDM) allergen, and in chronic HDM-driven allergic airway inflammation. As expected, acute responses to airway challenge with HDM, as well as type 2 inflammation and related features of airway remodeling during chronic HDM-induced allergic inflammation, were largely driven by DUOX1 with the respiratory epithelium. However, in the context of chronic HDM-driven inflammation, DUOX1 deletion in macrophages also significantly impaired type 2 cytokine production and indices of mucus metaplasia. Further studies revealed a contribution of macrophage-intrinsic DUOX1 in macrophage recruitment upon chronic HDM challenge, as well as features of macrophage activation that impact on type 2 inflammation and remodeling.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9391268PMC
http://dx.doi.org/10.1038/s41385-022-00530-xDOI Listing

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