Rat Model of Staphylococcal Enterotoxin B-Induced Rhinosinusitis.
- Author:
Seong Ki AHN
1
;
Sea Yuong JEON
;
Roza KHALMURATOV
;
Dong Ju KIM
;
Jin Pyeong KIM
;
Jeong Jae PARK
;
Dong Gu HUR
Author Information
- Publication Type:Original Article
- Keywords: Superantigen; Enterotoxin B; staphylococcal; Rat; Sprague-Dawley; Sinusitis; Histology
- MeSH: Animals; Enterotoxins; Eosinophils; Inflammation; Mucous Membrane; Nasal Cavity; Neutrophils; Nose; Rats; Sinusitis; T-Lymphocytes
- From:Clinical and Experimental Otorhinolaryngology 2008;1(1):24-28
- CountryRepublic of Korea
- Language:English
- Abstract: 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 microliter of SEB (100 microgram/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.
