Clin Exp Otorhinolaryngol.  2008 Mar;1(1):24-28. 10.3342/ceo.2008.1.1.24.

Rat Model of Staphylococcal Enterotoxin B-Induced Rhinosinusitis

Affiliations
  • 1Department of Otorhinolaryngology, Gyeong-Sang National University Hospital, Jinju, Korea. syjeon@nongae.gsnu.ac.kr

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.

Keyword

Superantigen; Enterotoxin B; staphylococcal; Rat; Sprague-Dawley; Sinusitis; Histology

MeSH Terms

Animals
Enterotoxins
Eosinophils
Inflammation
Mucous Membrane
Nasal Cavity
Neutrophils
Nose
Rats
Sinusitis
T-Lymphocytes
Enterotoxins

Figure

  • Fig. 1 Light micrographs of rats sacrificed at day 1. (A) Sinonasal air space bounded by septum, upper nasoturbinate and lower maxilloturbinate in section of control rats shows no evidence of inflammation (H&E, original ×40). (B) Inflammatory cell clusters are observed in sinonasal space of SEB-applied rats (H&E, original ×40). (C) Magnification of marked area on B reveals that the inflammatory cells in sinonasal air space are neutrophils (H&E, original ×400).

  • Fig. 2 Light micrographs of lamina propria under high magnification (H&E, original ×400) sacrificed at day 1. (A) Lamina propria of control rats shows rare cellular infiltration. (B) Extensive infiltration of neutrophils in lamina propria can be observed in SEB-applied rats.

  • Fig. 3 Ratio of the sinus spaces occupied by neutrophil clusters. Ratio of sinus spaces occupied by neutrophil clusters increased significantly at day 1 and regressed by day 5 (*P<0.05 on 2-tailed t-test, +P<0.05 on analysis of variance).

  • Fig. 4 Infiltrating neutrophils in the lamina propria. Significantly more neutrophils infiltrated the lamina propria at day 1 as shown by peak at day 1 (*P<0.05 on 2-tailed t-test, +P<0.05 on analysis of variance).


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