The Laryngoscope V C 2009 The American Laryngological, Rhinological and Otological Society, Inc. IgE Response to Staphylococcal Enterotoxins in Adenoid Tissues from Atopic Children Seung-Youp Shin, MD; Gil-Soon Choi, MD; Kun-Hee Lee, MD, PhD; Sung-Wan Kim, MD, PhD; Joong-Saeng Cho, MD, PhD; Hae-Sim Park, MD, PhD Objectives/Hypothesis: To evaluate local pro- duction of staphylococcal superantigen (SAg)-specific IgE in adenoid tissue and to compare its prevalence with that in the tonsil and serum, as well as its rela- tionship with markers of allergic inflammation within adenoid tissue. Study design: Prospective randomized study. Methods: We recruited 18 atopic children who had rhinitis symptoms and were sensitized to more than one common aeroallergen, and 22 nonatopic chil- dren undergoing adenotonsillectomy. Immunoassays were performed using adenoid tissue homogenate to quantify the levels of three staphylococcal SAg-spe- cific IgE (SEA, SEB, and TSST-1), total IgE, eosino- phil cationic protein (ECP), mast cell tryptase, and soluble CD23. Results: Three kinds of SAg-specific IgE were detected in the adenoid and tonsil tissues of atopic patients, but not in those of nonatopic patients. In atopic children, the prevalence of SEA-, SEB-, and TSST-1-specific IgE in adenoid tissues (61.1%, 27.8%, 33.3%, respectively) were higher than those in tonsil tissues (38.9%, 5.6%, 11.1%, respectively) and in sera (11.1%, 27.8%, 16.7%, respectively). Subjects with high SEA levels showed significantly higher serum and adenoid total IgE, with higher eosinophilia. Sig- nificant correlations were noted between SAg-specific IgE levels and tryptase levels in adenoid tissue. Conclusions: Local specific IgE response to staphylococcal SAgs, especially SEA may contribute to ongoing allergic inflammation in adenoid tissue from atopic children. Key Words: Staphylococcal superantigen, adenoid, atopy, eosinophil, mast cell. Laryngoscope, 119:171–175, 2009 INTRODUCTION The adenoids are believed to serve as a reservoir for pathogens responsible for several upper airway diseases. The predominant aerobic bacteria in the core tissue are a-hemolytic and c-hemolytic streptococci, Haemophilus influenzae, and Staphylococcus aureus, which are also known as etiologic pathogens in otitis media, rhinosinu- sitis, and adenotonsillitis. 1,2 Recently, there has been an increased interest in the potential role of adenoid tissue in atopic diseases. A few studies have shown that adenoids from atopic children have cellular and cytokine profiles that differ from those seen in nonatopic children, and that eosinophils could be involved in adenoid inflammation. 3,4 S. aureus is a human pathogen responsible for sev- eral infectious upper airway diseases. According to recent studies, staphylococcal enterotoxins (SEs) poten- tially play a role in the pathophysiology of atopic diseases. SEs are a large protein family composed of SEA to SEQ, along with toxic shock syndrome toxin-1 (TSST-1), all of which may act as superantigens (SAgs). These SAgs have the capacity to activate large popula- tions (5%–20%) of T cells through cross-linking MHC class II molecules on antigen-presenting cells (APCs) with a variable Vb region on T cell receptors, thus bypassing common antigen presentation mechanisms. 5 In addition to classic SAg effects, SAgs may also act as conventional allergens, inciting specific IgE responses in the serum. The presence of this SAg-specific IgE in serum is associated with severe atopic dermatitis (AD) and airway diseases such as asthma, rhinitis, and nasal polyps; 6–9 the conventional allergic reaction is believed to augment local SAg-mediated inflammation. Both mu- rine models and human studies have demonstrated Th2- type cytokine secretion and polyclonal IgE synthesis in response to SAg stimulation. 10,11 However, to the best of our knowledge, little effort has been expanded to detect local SAg-mediated inflammation in the respiratory mucosa of children. From the Department of Otolaryngology (S-Y.S., K-H.L., S-W.K., J-S.J.), Kyunghee University Hospital and Kyunghee University College of Medicine, Seoul, Korea; and Department of Allergy and Rheumatology (G-S.C., H-S.P .), Ajou University Hospital and Ajou University School of Medicine, Suwon, Korea. Editor’s Note: This Manuscript was accepted for publication July 15, 2008. This study was supported by a grant from the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (A030001 and A050571). Send correspondence to Hae-Sim Park, MD, PhD, Department of Allergy and Rheumatology, Ajou University, School of Medicine, Won- chondong San-5, Paldalgu, Suwon 442-749, Korea. E-mail: hspark@ajou. ac.kr DOI: 10.1002/lary.20046 Laryngoscope 119: January 2009 Shin et al.: SAg-Specific IgE in Adenoid Tissue 171