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    포도상 구균의 장독소 B에 의해 유발된 비부비동염 흰쥐모델에 관한 연구 = (The)rat model of rhinosinusitis induced by staphylococcal enterotoxin B

    한글로보기

    https://www.riss.kr/link?id=T10742975

    • 저자
    • 발행사항

      진주: 慶尙大學校, 2006

    • 학위논문사항

      학위논문(박사) -- 慶尙大學校 大學院 , 醫學科 , 2006

    • 발행연도

      2006

    • 작성언어

      한국어

    • 주제어
    • KDC

      511.56 판사항(4)

    • DDC

      616.014 판사항(21)

    • 발행국(도시)

      경상남도

    • 형태사항

      v, 33장: 삽화, 도표; 26 cm

    • 일반주기명

      참고문헌: 장 29-33

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      • 국립중앙도서관 국립중앙도서관 우편복사 서비스
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    부가정보

    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    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.
    번역하기

    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.

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    목차 (Table of Contents)

    • I. 서론 1
    • II. 대상 및 방법 5
    • 1. 흰쥐의 정상적인 비부비강 해부학적 구조 5
    • 1) 연구 대상 5
    • 2) 연구 방법 5
    • I. 서론 1
    • II. 대상 및 방법 5
    • 1. 흰쥐의 정상적인 비부비강 해부학적 구조 5
    • 1) 연구 대상 5
    • 2) 연구 방법 5
    • 2. 포도상 구균의 장독소 B에 의한 비부비동염 흰쥐 모델제작과 조직처리 7
    • 1) 연구 대상 7
    • 2) 연구 방법 7
    • 3) 조직에서 염증 소견의 광학현미경학적 관찰 8
    • 3. 통계분석 9
    • III. 결과 10
    • IV. 고찰 22
    • V. 결론 28
    • 참고문헌 29
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