The exact pathogenesis of chronic rhinosinusitis (CRS) has not been elucidated as yet. The major potential factors of CRS are known to be bacteria, allergy, fungi, and most recently, superantigens. Following the report in which Schubert hypothesized a...
The exact pathogenesis of chronic rhinosinusitis (CRS) has not been elucidated as yet. The major potential factors of CRS are known to be bacteria, allergy, fungi, and most recently, superantigens. Following the report in which Schubert hypothesized a potential unifying role for bacterial superantigens in the pathogenesis of CRS, a few clinical studies regarding causal relationship between
superantigens and CRS have been published. Superantigens can directly stimulate specific Vβ regions of the T-cell receptor and up-regulate as much as 30% of the body's lymphocytes. The exact role of superantigens in CRS, however, remains elusive. Several articles have reported severe or long-standing inflammatory tissue responses induced by superantigens in parts other than nose and paranasal sinuses, such as skin, lung, or gut in an animal model. But, no animal model of CRS has been reported up to date using superantigens. According to Schubert's hypothesis, it was postulated that chronic inflammation could occur when superantigens are applied intranasally. The aim of the present study was therefore to verify Schubert's hypothesis by investigating whether staphylococcal enterotoxin B (SEB) called superantigens could induce CRS in a rat model.
Forty ㎕ of 100 µg/mL of SEB was applied intranasally to 4~6 week-old Sprague-Dawley rats, and the same amount of phosphate buffered saline was applied to the control rats. At days 1, 5, 14 and 28 the rats were sacrificed and the nasal cavities and sinuses were prepared for histological investigation.
There was significant infiltration of neutrophils in the lamina propria of the respiratory epithelium, and significant appearance of inflammatory cell clusters in the sinuses air spaces in the SEB instilled rats. The rats sacrificed at day 1 showed significantly more neutrophilic inflammation. The amount of inflammation had decreased at days 5 and there was little evidence of inflammation at days 14 and 28.
In conclusion, intranasally applied SEB induced acute rhinosinusitis in rats, showing the highest peak at day 1. However, the expected evidences of chronic inflammation induced by superantigens were not observed. Contrary to Schubert's hypothesis, the presence of superantigens in the nose and paranasal sinuses alone could not induce CRS. It thus appears that multiple conditions or complex mechanisms might be involved in the pathogenesis of CRS.