490 Allergic chronic sinusitis (ACS) and nonallergic chronic sinusitis (NCS) are common causes of morbid- ity and exert a significant impact on the health care sys- tems of developed countries. 1 They are characterized by inflammatory mucosal thickening and polyp formation with a predominantly eosinophilic cellular infiltrate, 2 which is thought to be mediated by T cell–derived cytokines. Numerous in vitro studies support a role for Th-2 cytokines—IL-4, IL-5, and granulocyte-macrophage colony-stimulating factor (GM-CSF)—in this eosino- philia. We have recently shown that in allergic inflam- mation there is increased local expression of IL-4, 3 which is essential for isotype switching in favor of IgE Interleukin-4, interleukin-5, and granulocyte-macrophage colony-stimulating factor receptor expression in chronic sinusitis and response to topical steroids ERIN D. WRIGHT, MD, SAUL FRENKIEL, MD, KHALID AL-GHAMDI, MD, OMAR GHAFFAR, BSc, PETER SMALL, MD, TONY TROUTT, PhD, JAN TAVERNIER, PhD, and QUTAYBA HAMID, MD, PhD, Montreal, Canada, Seattle, Washington, and Ghent, Belgium Chronic sinusitis and its associated eosinophilic infiltrate are believed to be mediated, at least in part, by the upregulation of Th-2 cytokines, including interleukin-4, interleukin-5, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Interleukin-4 is involved in IgE production and in eosinophil recruitment through upregulation of vascular cell adhesion molecule-1. Interleukin-5 and GM-CSF are involved in eosinophil growth and survival. The aim of this study was to investigate the expression of receptors for these cytokines in the sinus mucosa of subjects with chronic sinusitis. Using the technique of in situ hybridization to detect specific cytokine receptor messenger RNA, we studied the sinus mucosa of subjects with nonallergic chronic sinusitis, subjects with allergic chronic sinusi- tis, subjects with allergic chronic sinusitis treated with topical steroids, and normal controls. Our data demonstrate higher expression of interleukin-4 receptor in subjects with allergic chronic sinusitis than in controls (p < 0.001) and higher expression of interleukin-5 receptor in both subjects with nonallergic chronic sinusitis and subjects with allergic chronic sinusi- tis than in controls (p < 0.001, p < 0.001). The expression of interleukin-4 receptor and inter- leukin-5 receptor was higher in subjects with allergic chronic sinusitis than in subjects with nonallergic chronic sinusitis (p < 0.001). GM-CSF receptor expression was also found to be higher in subjects with allergic chronic sinusitis and subjects with nonallergic chronic sinusitis than in controls (p < 0.001, p < 0.001). In contrast to interleukin-4 receptor and inter- leukin-5 receptor, however, expression of GM-CSF receptor was higher in subjects with non- allergic chronic sinusitis than in subjects with allergic chronic sinusitis (p < 0.001). In sub- jects with allergic chronic sinusitis treated with topical corticosteroids, the expression of interleukin-4 receptor and interleukin-5 receptor messenger RNA levels was significantly lower than levels in patients with allergic chronic sinusitis who were not taking topical steroids (p < 0.001, p < 0.001). Steroid treatment had no effect on GM-CSF receptor mes- senger RNA expression. In conclusion, our data support a role for Th-2 cytokine receptors in the pathophysiology of chronic sinusitis. Further, our data lend support to the theory that differential activation of distinct cytokine pathways mediates inflammation in chronic sinusitis depending on whether there is associated allergy. Finally, treatment with topical corticosteroids has been demonstrated in chronic sinusitis to downregulate receptors for interleukin-4 and interleukin-5. (Otolaryngol Head Neck Surg 1998;118:490-5.) From Meakins-Christie Laboratories (Drs. Wright, Al-Ghamdi, and Hamid and Mr. Ghaffar); McGill Nasal Research Group (Drs. Frenkiel, Small, and Hamid); the SMBD-Jewish General Hospital, McGill University, Montreal (Drs. Wright, Frenkiel, Al-Ghamdi, and Small); the Immunex Corp. (Dr. Troutt); and the Department of Biochemistry, University of Ghent, Belgium (Dr. Tavernier). Supported by the Network Center of Excellence for Respiratory Diseases and MRC, Canada. Recipient of the Sam Sanders Award for Best Paper in Basic Science at the Annual Meeting of the American Academy of Otolaryngic Allergy, Washington, D.C., Sept. 26-28, 1996. Reprint requests: Qutayba Hamid, MD, PhD, Meakins-Christie Laboratories, 3626 St. Urbain St., Montreal, Quebec, H2X 2P2, Canada. Copyright © 1998 by the American Academy of Otolaryngology– Head and Neck Surgery Foundation, Inc. 0194-5998/98/$5.00 + 0 23/1/80537