国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2015年
7期
497-503
,共7页
尹丽娟%王瑞雪%孙英%韩淑英
尹麗娟%王瑞雪%孫英%韓淑英
윤려연%왕서설%손영%한숙영
哮喘%补体%过敏毒素%C3a%C5a%气道重塑
哮喘%補體%過敏毒素%C3a%C5a%氣道重塑
효천%보체%과민독소%C3a%C5a%기도중소
Asthma%Complement%Anaphylatoxins%C3a%C5a%Remodelling
目的 探求补体成分过敏毒素C3a和C5a在支气管哮喘(简称哮喘)气道表达及对结构细胞的作用.方法 利用免疫组织化学的方法对补体成分C3、C3d、C5b-9、C3aR和C5aR在健康和哮喘气道黏膜的表达/沉积进行比较.结果 发现在哮喘患者气道黏膜标本中,上述成分在气道黏膜层、黏膜下层、平滑肌及腺体的表达/沉积明显增加.体外实验表明补体C3a和C5a均可刺激气道组织结构细胞(上皮、内皮、平滑肌和成纤维细胞)的增殖.结论 结果提示补体系统活化及过敏毒素C3a和C5a可能参与哮喘发病过程.
目的 探求補體成分過敏毒素C3a和C5a在支氣管哮喘(簡稱哮喘)氣道錶達及對結構細胞的作用.方法 利用免疫組織化學的方法對補體成分C3、C3d、C5b-9、C3aR和C5aR在健康和哮喘氣道黏膜的錶達/沉積進行比較.結果 髮現在哮喘患者氣道黏膜標本中,上述成分在氣道黏膜層、黏膜下層、平滑肌及腺體的錶達/沉積明顯增加.體外實驗錶明補體C3a和C5a均可刺激氣道組織結構細胞(上皮、內皮、平滑肌和成纖維細胞)的增殖.結論 結果提示補體繫統活化及過敏毒素C3a和C5a可能參與哮喘髮病過程.
목적 탐구보체성분과민독소C3a화C5a재지기관효천(간칭효천)기도표체급대결구세포적작용.방법 이용면역조직화학적방법대보체성분C3、C3d、C5b-9、C3aR화C5aR재건강화효천기도점막적표체/침적진행비교.결과 발현재효천환자기도점막표본중,상술성분재기도점막층、점막하층、평활기급선체적표체/침적명현증가.체외실험표명보체C3a화C5a균가자격기도조직결구세포(상피、내피、평활기화성섬유세포)적증식.결론 결과제시보체계통활화급과민독소C3a화C5a가능삼여효천발병과정.
Objective To investigate expression of complement components and anaphylatoxins C3a and C5a in bronchial mucosa of asthmatics and their effects on airways structural cells.Methods Immunohistochemistry was used to detect expression/deposition of complement components C3,C3d,C5b-9,C3aR and C5aR in bronchial mucosa of asthmatics compared with healthy controls,and as well as expression of C3aR and C5aR in vitro,an in vitro assays was employed to measure effects of C3R and C5a on proliferation of airways structural cells.Results Immunostaining showed that in asthmatic airways the immunoreactivity of above components was significantly elevated in the epithelium,submucosa,smooth muscles and gland.In vitro experiments indicated that airways structural cells expressed anaphylatoxin receptors C3aR and C5aR.Exposure of C3a and C5a induced the proliferation of these structural cells,including epithelial,endothelial,smooth muscle and fibroblast cells.Conclusions Data suggest that activation of the complement system and anaphylatoxins C3a and C5a may be involved in the pathogenesis of asthma.