Relationship between Staphylococcal superantigens and the dominant expression of T-cell receptor V beta gene in chronic rhinosinusitis with nasal polyp / 中华耳鼻咽喉头颈外科杂志

ABSTRACT

<p><b>OBJECTIVE</b>To analyse the relationship between superantigens produced by Staphylococcus aureus and the mRNA expression of T-cell receptor V beta region (TCR Vbeta), and to investigate the possible role of Staphylococcal superantigens in the pathogenesis of nasal polyps.</p><p><b>METHODS</b>Sinonasal mucus and polyp/mucosa tissue were obtained from patients with chronic rhinosinusitis (22 patients with bilateral nasal polyps, 15 without nasal polyps) and 12 normal subjects as comparative negative controls. Mucus specimens were assayed by enzyme-linked immunosorbent assay (ELISA) for Staphylococcal exotoxins,and analyzed for the expression of TCR Vbeta genes using the technique of reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The percentages of Staphylococcus exotoxins in nasal polyps were 54.54% (21/22) for chronic rhinosinusitis with nasal polyp (CRSwNP) subjects. There were no positive results in the CRSsNP or control groups. The expressional intensity of Vbeta3 (10.02), Vbeta14 (3.54), Vbeta15 (2.39), Vbeta17 (3.48), and Vbeta20 (2.94) was increased significantly for Staphylococcal exotoxin B (SEB) positive subjects (P < 0.05). Vbeta2 (13.8) and Vbeta6. 1-3 (6.53) were significantly highly expressed for toxic shock syndrome toxin-1 (TSTf-1) positive subjects in CRSwNP group (P < 0.05). There were no dominantly used Vbeta fragments in ELISA- negative specimens. In the group of chronic rhinosinusitis without nasal polyp (CRSsNP), most of TCR Vbeta gene subfamilies demonstrated a trend toward higher expressional levels compared with those of normal controls, although there was no statistical difference (P > 0.05).</p><p><b>CONCLUSIONS</b>There was relationship between Staphylococcal superantigens and the excursion of TCR Vbeta gene spectra in nasal polyp, and superantigens possibly play an important role in the pathogenesis of CRSwNP.</p>