Lower airway inflammation in patients with N-ERD is heterogeneous
Published: August 15, 2020
There is a subset of asthma patients whose symptoms are exacerbated by aspirin or other non-steroidal anti-inflammatory drugs (NSAID). This clinical phenotype, NSAIDs-exacerbated respiratory disease (N-ERD) is characterized by moderate to severe asthma and chronic eosinophilic rhinosinusitis with recurrent nasal polyps. Previous studies showed alterations in eicosanoid synthesis in N-ERD and overproduction of cysteinyl leukotrienes (CysLTs) along with a classical T2-inflammatory pattern in airway mucosa. These studies, however, relied usually on surrogate markers of lower airway inflammation.
In a recent study published in The Journal of Allergy and Clinical Immunology (JACI), Jakiela B et al. measured various cellular and molecular parameters in bronchoalveolar lavage fluid sampled in N-ERD patients and NSAID-tolerant asthmatics, and were thus able to investigate the inflammation directly at the level of lower airways.
This comprehensive approach revealed large diversity of lower airway inflammation in N-ERD, which was consistent with the heterogeneity of lower airway inflammation observed in the general asthma population. Classical T2-inflammation with airway eosinophilia and increased CysLTs production was present in over half of N-ERD patients, while the remaining patients showed more heterogeneous pattern and variable degrees of airway neutrophilia.
The absence of a T2-pattern in lower airways in a subset of N-ERD patients suggests that upper airway inflammation still constitutes an important source of eosinophils and CysLTs, thus explaining the persistence of NSAIDs-hypersensitivity. This study also explains why therapies targeted at T2-inflammation may not be universally effective for controlling of asthma symptoms in N-ERD patients.
The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.
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