Expression of interleukin (IL)-12 (p40) and IL-12 (beta(2)) receptors in allergic rhinitis and chronic sinusitis

Citation
Ed. Wright et al., Expression of interleukin (IL)-12 (p40) and IL-12 (beta(2)) receptors in allergic rhinitis and chronic sinusitis, CLIN EXP AL, 29(10), 1999, pp. 1320-1325
Citations number
20
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
CLINICAL AND EXPERIMENTAL ALLERGY
ISSN journal
09547894 → ACNP
Volume
29
Issue
10
Year of publication
1999
Pages
1320 - 1325
Database
ISI
SICI code
0954-7894(199910)29:10<1320:EOI((A>2.0.ZU;2-W
Abstract
Background Interleukin (IL)-12 is a relatively new and structurally distinc t TH1-associated cytokine produced by B cells and macrophages, which may pl ay a suppressive role in the development of allergic sinonasal mucosal resp onses. Objective We investigated the expression of IL-12 (inducible p40 subunit) a nd its receptor (IL-12R beta(2) subunit) in tissue biopsies of naturally ex posed patients with allergy-associated (ACS) and nonallergy-associated chro nic 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 co rticosteroids on IL-12 and IL-12R expression was assessed. Methods To detect IL-12. and IL-12R mRNA, we employed the technique of in s itu hybridization using digoxigenin-labelled riboprobes. Results In both ACS and NCS subjects there was decreased expression of IL-1 2 as compared with control (P < 0.05). IL-12R (beta(2)) expression was decr eased in ACS subjects as compared with control (P<0.05), however, there was no significant difference found between NCS subjects and control. In the a llergen challenge subjects, there was a significant decrease in IL-12 expre ssion following challenge (P < 0.05). This effect was abrogated by pretreat ment of the subjects with topical corticosteroids. However, IL-12R (beta(2) ) expression showed no change following allergen challenge while pretreatme nt with topical corticosteroids resulted in increased expression of the (be ta(2)) receptor after allergen challenge (P < 0.05). Conclusion Our data suggest that IL-12 plays a role in the in vivo suppress ion of the allergic inflammatory response and that the control of this supp ression may be exerted largely via the IL-12 (beta(2)) receptor.