Superantigen-induced glucocorticoid insensitivity in the recurrence of chronic rhinosinusitis with nasal polyps.

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.