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Aspirin-exacerbated respiratory disease.
Hannah Wangberg1, Andrew A White1
1Division of Allergy, Asthma, and Immunology, Scripps Clinic, San Diego, CA, United States.
Current Opinion in Immunology
|April 17, 2020
Summary
Aspirin-exacerbated respiratory disease (AERD) involves immune system dysfunction, leading to severe asthma and inflammation. Understanding AERD
Area of Science:
- Immunology
- Respiratory Medicine
- Inflammation Research
Background:
- Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, nasal polyposis, and reactions to cyclooxygenase (COX)-1 inhibitors.
- Immune dysregulation in AERD includes reduced prostaglandin E2 (PGE2) and increased cysteinyl leukotrienes (CysLTs) and interleukin 33 (IL-33).
Purpose of the Study:
- To review the current understanding of the immunopathogenesis of Aspirin-exacerbated respiratory disease (AERD).
Main Methods:
- Literature review of recent advances in AERD research.
- Analysis of immune mediators and cellular pathways involved in AERD.
Main Results:
- AERD involves diminished prostaglandin E2 (PGE2) function and elevated cysteinyl leukotrienes (CysLTs) and IL-33.
- Inflammatory mediators promote the recruitment and activation of innate lymphoid cells type 2 (ILC2), mast cells, eosinophils, and leukocytes.
- These processes contribute to a cycle of type 2 inflammation in AERD.
Conclusions:
- Aspirin-exacerbated respiratory disease (AERD) pathogenesis is complex, involving multiple immune system components.
- Further research into AERD immunopathogenesis may reveal new therapeutic targets.
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