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摘要
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) alpha and beta, and the GR beta/GR alpha 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 GR beta in 3 CRS groups and controls were significantly different (all P < .05), and a similar increasing tendency of the GR beta/GR alpha ratio was found among groups besides the comparison of CRSwNP versus recurrent NP groups (P = .053). Furthermore, there was a clear trend of increased GR beta expression in the enzyme-linked immunosorbent assay (ELISA)-positive samples compared with ELISA-negative samples. Concerning GR alpha, the expression was enhanced significantly just in toxin-positive recurrent NP versus controls (P = .048), but the relative induction of GR beta was much higher, thereby leading to a higher GR beta/GR alpha ratio. Conclusions. Bacterial superantigens may contribute to glucocorticoid insensitivity through induction of GR beta, which appears to be a marker of steroid insensitivity in CRSwNP.
- 出版日期2011-11
- 单位山东大学
