RANTES, eotaxin and eotaxin-2 expression and production in patients with aspirin triad.
BACKGROUND
Polyposis, asthma, aspirin-intolerance and aspirin-triad are mostly accompanied with eosinophilia of mucosal airways. Chemotactic cytokines, the CC-chemokines regulated on activation, normal T-cell expressed (RANTES), eotaxin, and eotaxin-2 activate and attract eosinophilic leukocytes to the site of inflammation. This points to the implication of CC-chemokines in eosinophilia of nasal tissue of these diseases.


METHODS
Therefore, nasal polypous tissue specimens of patients suffering from chronic nasal polypous sinusitis (NP), intrinsic asthma (ATA), aspirin-intolerance (AINA), and aspirin-triad (TRIAD) were investigated. The amount of mRNA and protein of CC-chemokines was analyzed using semi-quantitative reverse transcriptase polymerase chain reaction and chemokine-specific enzyme-immuno-assays. The patterns of CC-chemokines were compared.


RESULTS
The mRNA-expression as well as protein synthesis of CC-chemokines was quantified in all tissues investigated. The expression of RANTES-mRNA in NP, ATA, AINA, and TRIAD (averaging 148-324% D-glyceraldehyde-3-phosphate dehydrogenase) and protein synthesis (0.13-0.15 ng/mg tissue weight) did not differ significantly. But the protein synthesis of eotaxin- and eotaxin-2-mRNA was significantly (P < 0.05) higher in TRIAD (3.3 pg/mg and 3.4 ng/mg tissue weight) (4 ng/mg tissue weight), than in NP, ATA, or AINA (1.8 pg/mg and 2.1 ng/mg, 2.1 pg/mg and 1.6 ng/mg, or 1.7 pg/mg and 2.2 ng/mg tissue weight, respectively).


CONCLUSIONS
Patients suffering from TRIAD in association with tissue eosinophilia were characterized by elevated eotaxin and eotaxin-2 mRNA-expression as well as protein-synthesis. This pointed to the implication of eotaxins and RANTES in eosinophilia-associated diseases. Further studies will have to prove, whether the analysis of these chemokines might improve the diagnosis of eosinophilia associated polyposis and initiate the development of new therapeutic strategies.
Pods
R
R
Department of Otorhinolaryngology, Head- and Neck-Surgery, University Kiel, Kiel, Germany.
Ross
D
D
van Hülst
S
S
Rudack
C
C
Maune
St
S
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin / Q000009:adverse effects*; D001249:Asthma / Q000150:complications / Q000276:immunology / Q000378:metabolism*; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D018946:Chemokine CCL5 / Q000096:biosynthesis* / Q000235:genetics; D019742:Chemokines, CC / Q000096:biosynthesis* / Q000235:genetics; D002631:Chemotactic Factors, Eosinophil / Q000096:biosynthesis / Q000235:genetics; D002908:Chronic Disease; D018076:DNA, Complementary / Q000096:biosynthesis; D004342:Drug Hypersensitivity / Q000150:complications / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis
C515456:CCL11 protein, human; C515484:CCL24 protein, human; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D018946:Chemokine CCL5; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D018076:DNA, Complementary; D012333:RNA, Messenger; D001241:Aspirin