Cellular responses to Staphylococcus aureus alpha-toxin in chronic rhinosinusitis with nasal polyps

Mitsuhiro Okano, Tazuko Fujiwara, Shin Kariya, Takaya Higaki, Takenori Haruna, Osamu Matsushita, Yohei Noda, Seiichiro Makihara, Kengo Kanai, Yasuyuki Noyama, Masami Taniguchi, Kazunori Nishizaki

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background: In contrast to Staphylococcus aureus-derived superantigenic exotoxins, the role of nonsuperantigenic exotoxins in the pathogenesis of eosinophilic airway diseases remains obscure. We sought to characterize S. aureus alpha-toxin-induced cellular responses in chronic rhinosinusitis with nasal polyps (CRSwNP).

Methods: Dispersed nasal polyp cells and uncinate tissue cells were prepared from patients with CRS with and without nasal polyps, respectively. Cells were incubated with various concentrations of alpha-toxin or staphylococcal enterotoxin B and then the levels of IL-5, IL-13, IFN-γ, IL-17A, and IL-10 in the cell supernatants were determined. The pathophysiological significance of alpha-toxin-induced cytokine production was also determined including radiological severity of rhinosinusitis, tissue and blood eosinophilia, serum total IgE level, and 1-s forced expiratory volume[1]forced vital capacity ratio (FEV1/FVC).

Results: Nasal polyp cells produced substantial amounts of IL-5, IL-13, IFN-γ, IL-17A, and IL-10 in response to alpha-toxin. Cytokine production was higher in nasal polyp cells than in uncinate tissue cells. The potency of alpha-toxin in stimulating IL-5, IL-13, and IL-10 production was comparable to that of enterotoxin. Alpha-toxininduced IFN-γ, IL-17A, and IL-10 production significantly and negatively correlated with the degree of eosinophil infiltration into nasal polyps. Conversely, alpha-toxin-induced IFN-γ and IL-10 production significantly and positively correlated with FEV1/FVC. IL-10 production was significantly lower in asthmatic patients compared to non-asthmatics

Conclusions: S. aureus-derived alpha-toxin can provoke cellular responses in nasal polyps. These responses, especially failure to synthesize IL-10, may play a role in the pathophysiology of CRSwNP.

Original languageEnglish
Pages (from-to)563-573
Number of pages11
JournalAllergology International
Volume63
Issue number4
DOIs
Publication statusPublished - Jan 1 2014

Keywords

  • Alpha-toxin
  • Chronic rhinosinusitis
  • Eosinophil
  • IL-10
  • Nasal polyps

ASJC Scopus subject areas

  • Immunology and Allergy

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