Aspirin exacerbated respiratory disease (AERD): molecular and cellular diagnostic & prognostic approaches

Aspirin-exacerbated respiratory disease (AERD) is characterized by immune cells dysfunction. This study aimed to investigate the molecular mechanisms involved in AERD pathogenesis. Relevant literatures were identified by a PubMed search (2005-2019) of english language papers using the terms Aspirin-exacerbated respiratory disease, Allergic inflammation, molecular mechanism and mutation. According to the significant role of inflammation in AERD development, ILC-2 is known as the most important cell in disease progression. ILC-2 produces cytokines that induce allergic reactions and also cause lipid mediators production, which activates mast cells and basophils, ultimately. Finally, Monoclonal antibody and Aspirin desensitization in patients can be a useful treatment strategy for prevention and treatment.

Automated summary

AERD is characterized by immune cells dysfunction, with ILC-2 playing a significant role in disease progression by producing cytokines that induce allergic reactions and activate mast cells and basophils, ultimately exacerbating the condition. Monoclonal antibody therapy and Aspirin desensitization have been identified as potential treatment strategies for prevention and management.