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Objectives. It has been proposed that microbial persistence, superantigen (SA) production, and host T-cell response may be involved in the development of chronic rhinosinusitis. According to the SA hypothesis, a single intranasal application of SA such as staphylococcal enterotoxin B (SEB) may induce chronic eosinophilic rhinosinusitis. This study aimed to develop a rat model of rhinosinusitis induced by intranasally applied SEB. Methods. Forty L of SEB (100 g/mL) or phosphate buffered saline was applied intranasally through each naris in 4 weekold Sprague-Dawley test rats (N=36) and controls (N=16), respectively. Following sacrifice at 1, 5, 14, and 28 days, the obtained nasal cavity and sinuses were prepared for histologic investigation. The histologic sections were examined in a blind manner for the ratio of the sinus spaces occupied by inflammatory cell clusters and the number of inflammatory cells in the lamina propria. Results. Infiltration of neutrophils in the lamina propria and appearance of neutrophil clusters in the sinus spaces were observed in the SEB-applied rats. The ratio of the sinus spaces occupied by neutrophil clusters and the number of neutrophils infiltrated in the lamina propria increased significantly at day 1 as compared with the control rats. Conclusion. Intranasally applied SEB induces acute neutrophilic rhinosinusitis in rats. Eosinophilic inflammation was not demonstrated. The mere presence of SA in the nose does not necessarily induce SA-induced inflammation, as suggested by the SA hypothesis.


Objectives. It has been proposed that microbial persistence, superantigen (SA) production, and host T-cell response may be involved in the development of chronic rhinosinusitis. According to the SA hypothesis, a single intranasal application of SA such as staphylococcal enterotoxin B (SEB) may induce chronic eosinophilic rhinosinusitis. This study aimed to develop a rat model of rhinosinusitis induced by intranasally applied SEB. Methods. Forty L of SEB (100 g/mL) or phosphate buffered saline was applied intranasally through each naris in 4 weekold Sprague-Dawley test rats (N=36) and controls (N=16), respectively. Following sacrifice at 1, 5, 14, and 28 days, the obtained nasal cavity and sinuses were prepared for histologic investigation. The histologic sections were examined in a blind manner for the ratio of the sinus spaces occupied by inflammatory cell clusters and the number of inflammatory cells in the lamina propria. Results. Infiltration of neutrophils in the lamina propria and appearance of neutrophil clusters in the sinus spaces were observed in the SEB-applied rats. The ratio of the sinus spaces occupied by neutrophil clusters and the number of neutrophils infiltrated in the lamina propria increased significantly at day 1 as compared with the control rats. Conclusion. Intranasally applied SEB induces acute neutrophilic rhinosinusitis in rats. Eosinophilic inflammation was not demonstrated. The mere presence of SA in the nose does not necessarily induce SA-induced inflammation, as suggested by the SA hypothesis.