CCL4 Levels Differ between Aspirin-Tolerant and Aspirin-Intolerant Patients with Asthma

Abstract

Aspirin-exacerbated respiratory disease (AERD) is an asthma phenotype characterized by nasal polyps, chronic hypertrophic eosinophilic sinusitis, asthma, and sensitivity to aspirin. Unawareness of this disease by patients and their physicians may have serious consequences because of the risk of near-fatal asthma. Its confirmative diagnosis can be established only by provocative aspirin challenge, which represents a potential risk for patient health. Purpose: Because CCL4 plays an important role in several pulmonary conditions, we tested its immunoreactivity in nasal lavages and sera from control subjects, and from aspirin-sensitive and non-aspirin-sensitive patients. Method: Immunoreactivity of CCL4 was measured in serum and nasal lavages from 30 healthy controls (HC), 23 patients with AERD, and 20 patients with aspirin-tolerant asthma (ATA). Additionally, a serum biobank contained sera from 90 HC, 83 patients with AERD, and 69 patients with ATA was employed. Results: The serum immunoreactivity of CCL4 could distinguish both types of asthma phenotypes. Conclusion: CCL4 may play an unexpected role in thephysiopathology of AERD.

Cytokines in serum, nasal secretion and exhaled breath condensate during mepolizumab therapy in patients with different phenotypes of severe eosinophilic asthma: A pilot study

“…One recent study showed that MIP-1β level was higher in N-ERD patients than in NSAIDs tolerant asthmatics in serum and nasal lavage; however, they included N-ERD subjects with significantly higher FEV1% than N-TA, which suggests that they were not matched according the disease severity. 10 It is noteworthy that we also observed higher levels of MIP-1β in the nasal samples in N-ERD than in N-TA subjects at both visits, although these differences were not statistically significant. In conclusion, it seems that MIP-1β may be an interesting marker of eosinophilic asthma depending on the severity of the disease and its phenotype; however, this observations should be further explored.…”

“…In the study of Suzukawa M et al, 6 clinical response to mepolizumab was correlated with the serum MIP‐1 β, and patients with lower baseline levels of this chemokine had a worse response to the treatment. One recent study showed that MIP‐1β level was higher in N‐ERD patients than in NSAIDs tolerant asthmatics in serum and nasal lavage; however, they included N‐ERD subjects with significantly higher FEV1% than N‐TA, which suggests that they were not matched according the disease severity 10 . It is noteworthy that we also observed higher levels of MIP‐1β in the nasal samples in N‐ERD than in N‐TA subjects at both visits, although these differences were not statistically significant.…”