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Nuclear factor‐κB activity is down‐regulated in nasal polyps from aspirin‐sensitive asthmatics
Author(s) -
Picado C.,
Bioque G.,
RocaFerrer J.,
Pujols L.,
Mullol J.,
Benitez P.,
Bulbena O.
Publication year - 2003
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.2003.23792.x
Subject(s) - nasal polyps , aspirin , medicine , messenger rna , electrophoretic mobility shift assay , gastroenterology , asthma , endocrinology , gene expression , chemistry , biochemistry , gene
Background: We examined whether a decreased activity of nuclear factor(NF)‐κB), a transcriptional regulator of cyclooxygenase‐2 (COX‐2), could account for down‐regulation of COX‐2 in nasal polyps of aspirin‐sensitive asthmatics. Methods: Nasal polyps were obtained from 17 aspirin‐intolerant asthma/rhinitis patients (AIAR; 7 men, mean age 48 ± 12 years) and 23 aspirin‐tolerant asthma/rhinitis patients (ATAR; 12 men, mean age 65 ± 11 years). COX‐2 mRNA expression was measured using semiquantitative reverse transcriptase competitive polymerase chain reaction (RT‐PCR), and the results were expressed as mean ± standard error of 10 6 molecules of mRNA/µg of total RNA. NF‐κB binding was measured with 32 P‐labeled oligonucleotides and electrophoretic mobility shift assay (EMSA), and the results were expressed as a percentage with respect to the mean EMSA obtained in 19 healthy nasal mucosa. Results: The mean levels of COX‐2 mRNA expression (0.25 ± 0.06) and NF‐κB activity (89 ± 13) in nasal polyps from AIAR were significantly lower than in polyps from ATAR (COX‐2 = 1.58 ± 0.50, and NF‐κB = 143 ± 12, P < 0.01 and P < 0.05, respectively). Levels of COX‐2 mRNA and NF‐κB activity in polyps from patients on corticosteroid therapy did not differ statistically from those who were not on this therapy before polypectomy. Conclusion: This study shows that the low expression of COX‐2 mRNA in nasal polyps from aspirin‐sensitive patients is associated with a down‐regulation of NF‐κB activity.