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Evaluation of Respiratory System Mechanics in Mice using the Forced Oscillation Technique
Published on: May 15, 2013
Upper airways in aspirin-exacerbated respiratory disease
Jeong-Hee Choi1, Ji-Hye Kim, Hae-Sim Park
1aDepartment of Pulmonology and Allergy, Hallym University Dongtan Sacred Heart Hospital, Hwaseong bDepartment of Allergy and Clinical Immunology, Ajou University Hospital, Suwon, Korea.
Purpose Of Review:
This review updates the status of chronic rhinosinusitis with nasal polyps (CRSwNP) in aspirin-exacerbated respiratory disease (AERD) in the contexts of epidemiology, diagnosis, pathogenesis, and treatment.
Recent Findings:
Recent studies have shown that prostaglandin E₂ (PGE₂) deficiency induces an AERD phenotype in PGE₂ synthase-1 knock-out mice and also PGE₂ resistance in granulocytes of AERD patients. The numbers of platelet-adherent leukocytes increase in AERD patients, enhancing production of cysteinyl leukotrienes (CysLTs) via transcellular metabolism of arachidonate. INF-γ released from eosinophils of the sinus tissue of AERD patients promotes eosinophil maturation, increases leukotriene-associated gene expression, and releases CysLTs. The serum periostin level has been suggested to be a useful biomarker predicting the AERD/CRSwNP phenotype. Aspirin desensitization was reported to decrease the levels of CD4⁺ T cell-derived cytokines, including INF-γ and IL-10, in line with the newly defined role of INF-γ in AERD.
Summary:
Recent findings further support the notion that arachidonic acid metabolism is dysregulated in AERD patients. This is reflected by resistance to PGE₂, overproduction of CysLTs by enhanced numbers of platelet-adherent leukocytes, and cellular stimulation by INF-γ released from eosinophils. Aspirin desensitization may be a useful treatment option in AERD patients exhibiting recalcitrant CRSwNP.
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