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Expression of interleukin (IL)‐12 (p40) and IL‐12 (β 2 ) receptors in allergic rhinitis and chronic sinusitis
Author(s) -
Wright Ed,
Pota Christodoulopoulos,
Saul Frenkiel,
Qutayba Hamid
Publication year - 1999
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2222.1999.00637.x
Subject(s) - medicine , in situ hybridization , receptor , allergy , allergen , immunology , interleukin , interleukin 4 , cytokine , gene expression , biology , gene , biochemistry
Background Interleukin (IL)‐12 is a relatively new and structurally distinct TH1‐associated cytokine produced by B cells and macrophages, which may play a suppressive role in the development of allergic sinonasal mucosal responses. Objective We investigated the expression of IL‐12 (inducible p40 subunit) and its receptor (IL‐12R β 2 subunit) in tissue biopsies of naturally exposed patients with allergy‐associated (ACS) and nonallergy‐associated chronic sinusitis (NCS) and compared it with controls. We also examined IL‐12 and IL‐12R expression in biopsies from a ragweed allergen challenge model. In the allergen challenge model, the effect of pretreatment with topical corticosteroids on IL‐12 and IL‐12R expression was assessed. Methods To detect IL‐12 and IL‐12R mRNA, we employed the technique of in situ hybridization using digoxigenin‐labelled riboprobes. Results In both ACS and NCS subjects there was decreased expression of IL‐12 as compared with control ( P < 0.05). IL‐12R (β 2 ) expression was decreased in ACS subjects as compared with control ( P < 0.05), however, there was no significant difference found between NCS subjects and control. In the allergen challenge subjects, there was a significant decrease in IL‐12 expression following challenge ( P < 0.05). This effect was abrogated by pretreatment of the subjects with topical corticosteroids. However, IL‐12R (β 2 ) expression showed no change following allergen challenge while pretreatment with topical corticosteroids resulted in increased expression of the (β 2 ) receptor after allergen challenge ( P < 0.05). Conclusion Our data suggest that IL‐12 plays a role in the in vivo suppression of the allergic inflammatory response and that the control of this suppression may be exerted largely via the IL‐12 (β 2 ) receptor.