Objective. To investigate a potential mechanism by which superantigens could induce glucocorticoid insensitivity in chronic rhinosinusitis (CRS) patients. Study Design. Prospective cohort study. Setting. Tertiary medical center. Subjects and Methods. Sinonasal polyps were obtained from CRS patients with nasal polyps (CRSwNP; 20 without recurrence, 18 with recurrent NP followed for 1.5-2.0 years) and nasal mucosa from 16 CRS patients without nasal polyps (CRSsNP). Specimens were tested by enzyme-linked immunosorbent assay for staphylococcal exotoxins (SEs) including SEA, SEB, SEC, SED, and toxic shock syndrome toxin type-1 (TSST-1) and assessed by immunohistochemistry for glucocorticoid receptor (GR) α and β, and the GRβ/GRα ratio was analyzed. Results. In CRSwNP, 13 of 18 (72.22%) subjects with subsequently recurrent NP, 11 of 20 (55.00%) subjects without NP recurrence, and 1 of 16 (6.25%) CRSsNP subjects with positive reactions for SEs were obtained. There were no positive results in controls. The expressions of GRβ in 3 CRS groups and controls were significantly different (all P < .05), and a similar increasing tendency of the GRβ/GRα ratio was found among groups besides the comparison of CRSwNP versus recurrent NP groups ( P = .053). Furthermore, there was a clear trend of increased GRβ expression in the enzyme-linked immunosorbent assay (ELISA)–positive samples compared with ELISA-negative samples. Concerning GRα, the expression was enhanced significantly just in toxin-positive recurrent NP versus controls ( P = .048), but the relative induction of GRβ was much higher, thereby leading to a higher GRβ/GRα ratio. Conclusions. Bacterial superantigens may contribute to glucocorticoid insensitivity through induction of GRβ, which appears to be a marker of steroid insensitivity in CRSwNP.
Competitive, enzyme-linked immunosorbent assay for toxic shock syndrome toxin 1.
