ArticleFrontiers in immunology2025
The relationship of chemokine levels and the type of symptoms caused by NSAIDs or alcohol in patients with NSAIDs-exacerbated respiratory disease.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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Corrections and comments
- Erratum issued
Authors and funding
4 authors.
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Abstract
Introduction: Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is an asthma phenotype with a complex pathogenesis involving chemokine-mediated inflammation. This study aimed to evaluate the association between chemokine levels and symptoms triggered by NSAIDs and alcohol in patients with N-ERD. Methods: Seventy-two subjects (41 N-ERD, 20 NSAID-tolerant asthma [NTA], and 11 healthy controls) were assessed via questionnaire, lung function tests, and measurement of selected chemokines in serum, urine, and exhaled breath condensate (EBC). Results: N-ERD patients exhibited significantly higher CCL17/TARC levels in EBC compared to controls (p<0.001). Both N-ERD and NTA groups had elevated serum CCL5/RANTES levels relative to controls (p=0.002 and p=0.04, respectively). Respiratory symptoms after alcohol consumption were reported by 48% of N-ERD patients, significantly more frequent than in controls (p<0.05), with dyspnea more common in N-ERD than NTA (p=0.03). In N-ERD patients, serum CCL17/TARC levels were lower in those experiencing dyspnea after NSAIDs (p=0.03), while serum CXCL10/IP-10 levels were higher in patients with mixed (not only respiratory) symptoms (p=0.015). Alcohol symptoms in N-ERD correlated with lower urinary CCL5/RANTES levels (p=0.01). Nasal blockage after alcohol was associated with reduced CCL17/TARC in EBC (p=0.01), and dyspnea after alcohol correlated with lower serum CCL26/Eotaxin-3 (p=0.047). Conclusion: Chemokine profiles differ according to symptom type following NSAID or alcohol exposure in N-ERD patients. These findings highlight the heterogeneity of N-ERD and suggest distinct inflammatory pathways linked to clinical presentations.
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