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. 2006 Oct;20(20):914-6.

[A primary study about the correlation between superantigens produced by Staphylococcus aureus and chronic rhinosinusitis with nasal polyps]

[Article in Chinese]
Affiliations
  • PMID: 17225516

[A primary study about the correlation between superantigens produced by Staphylococcus aureus and chronic rhinosinusitis with nasal polyps]

[Article in Chinese]
Mingming Wang et al. Lin Chuang Er Bi Yan Hou Ke Za Zhi. 2006 Oct.

Abstract

Objective: To study the role of superantigens produced by Staphylococcus aureus in the pathogenesis of nasal polyps.

Method: sinonasal mucus and polyp/mucosa tissue were obtained from sixty-nine patients with chronic rhinosinusitis (42 patients with bilateral nasal polyps, 27 without nasal polyps). Samples from twelve normal subjects were also obtained for comparative negative controls. Mucus specimens were cultured for bacteria. Tissue specimens were assayed by ELISA for staphylococcal exotoxins. In addition, the histopathology of nasal polyps was studied. The paraffin sections were stained with hematoxylin and eosin, and these were examined for eosinophil counts.

Result: The percentages of Staphylococcus aureus in sinonasal mucus were 7.1 for chronic rhinosinusitis with nasal polyp (CRSwNP) subjects, 3.7% for chronic rhinosinusitis without nasal polyps (CRSsNP). and 0 for controls respectively. There were no significant differences between these groups. In CRSwNP subjects 23 of 42 samples (54.76%) demonstrated reactivity for at least one staphylococcal exotoxin. There were no positive results in the CRSsNP or control groups. The mean eosinophil counts were 23. 94+/-13. 88 in CRSwNP group, 0.29+/-0.51 in CRSsNP group, and 0. 08+/-0.28 in controls. The differences in these three groups were all significant ( P <0.05). There was a trend toward higher eosinophil levels in polyps of ELISA-positive patients compared with that of ELISA-negative patients, although this was not statistically different ( P >0.05).

Conclusion: There were correlation between Staphylococcal superantigens and nasal CRSwNP, and superantigens were possible etiological agents in the pathogenesis of CRSwNP.

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