中国组织化学与细胞化学杂志
中國組織化學與細胞化學雜誌
중국조직화학여세포화학잡지
CHINESE JOURNAL OF HISTOCHEMISY AND CYTOCHEMISY
2001年
1期
76-80
,共5页
刘建%彭东信%刘晓晴%朱朝霞%车东媛%赵时宇
劉建%彭東信%劉曉晴%硃朝霞%車東媛%趙時宇
류건%팽동신%류효청%주조하%차동원%조시우
肺炎支原体%肺间质纤维化%血小板源性生长因子-BB%免疫组织化学%大鼠
肺炎支原體%肺間質纖維化%血小闆源性生長因子-BB%免疫組織化學%大鼠
폐염지원체%폐간질섬유화%혈소판원성생장인자-BB%면역조직화학%대서
为探讨血小板源性生长因子-BB(PDGF-BB)在肺炎支原体反复肺感染导致肺间质纤维化的发病机制中的作用,作者于24周内给大鼠反复9次吸入肺炎支原体复制慢性肺感染模型。随后用PDGF-BB单克隆抗体按SABC法行免疫组织化学染色和定量图像分析,以观察肺组织PDGF-BB蛋白质水平表达的变化。结果显示:(1)感染组动物(n=4)支气管肺泡灌洗液肺炎支原体-PCR检测均为阳性,而对照组(n=4)和感染加红霉素治疗组动物(n=4)均为阴性(P<0.05);三组动物的支气管和肺组织常规细菌培养结果均为阴性;感染组动物透射电镜检查见肺泡间隔增宽,其中有较多胶原纤维堆积,其余两组则未见明显异常。(2)感染组动物肺间质结缔组织内、支气管壁和小血管壁内可见较强的PDGF-BB阳性染色,其积分光密度为37.90±10.14(n=4),显著高于对照组者(7.54±1.98,n=4,P<0.05)和感染加红霉素治疗组者(10.90±3.30,n=4,P<0.05)。提示肺炎支原体反复肺感染的PDGF-BB蛋白质水平表达增加,可能参与肺间质纤维化的发病过程。
為探討血小闆源性生長因子-BB(PDGF-BB)在肺炎支原體反複肺感染導緻肺間質纖維化的髮病機製中的作用,作者于24週內給大鼠反複9次吸入肺炎支原體複製慢性肺感染模型。隨後用PDGF-BB單剋隆抗體按SABC法行免疫組織化學染色和定量圖像分析,以觀察肺組織PDGF-BB蛋白質水平錶達的變化。結果顯示:(1)感染組動物(n=4)支氣管肺泡灌洗液肺炎支原體-PCR檢測均為暘性,而對照組(n=4)和感染加紅黴素治療組動物(n=4)均為陰性(P<0.05);三組動物的支氣管和肺組織常規細菌培養結果均為陰性;感染組動物透射電鏡檢查見肺泡間隔增寬,其中有較多膠原纖維堆積,其餘兩組則未見明顯異常。(2)感染組動物肺間質結締組織內、支氣管壁和小血管壁內可見較彊的PDGF-BB暘性染色,其積分光密度為37.90±10.14(n=4),顯著高于對照組者(7.54±1.98,n=4,P<0.05)和感染加紅黴素治療組者(10.90±3.30,n=4,P<0.05)。提示肺炎支原體反複肺感染的PDGF-BB蛋白質水平錶達增加,可能參與肺間質纖維化的髮病過程。
위탐토혈소판원성생장인자-BB(PDGF-BB)재폐염지원체반복폐감염도치폐간질섬유화적발병궤제중적작용,작자우24주내급대서반복9차흡입폐염지원체복제만성폐감염모형。수후용PDGF-BB단극륭항체안SABC법행면역조직화학염색화정량도상분석,이관찰폐조직PDGF-BB단백질수평표체적변화。결과현시:(1)감염조동물(n=4)지기관폐포관세액폐염지원체-PCR검측균위양성,이대조조(n=4)화감염가홍매소치료조동물(n=4)균위음성(P<0.05);삼조동물적지기관화폐조직상규세균배양결과균위음성;감염조동물투사전경검사견폐포간격증관,기중유교다효원섬유퇴적,기여량조칙미견명현이상。(2)감염조동물폐간질결체조직내、지기관벽화소혈관벽내가견교강적PDGF-BB양성염색,기적분광밀도위37.90±10.14(n=4),현저고우대조조자(7.54±1.98,n=4,P<0.05)화감염가홍매소치료조자(10.90±3.30,n=4,P<0.05)。제시폐염지원체반복폐감염적PDGF-BB단백질수평표체증가,가능삼여폐간질섬유화적발병과정。
In order to investigate the role of platelet derived growthfactor-BB(PDGF-BB) in the pathogenesis of pulmonary interstitial fibrosis in rats repeatedly infected by mycoplasma pneumoniae (MP), the authors established a chronic pulmonary infected rat model by indhaling MP for 9 times in 24 weeds. Then immunohistochemical stain was performed with PDGF-BB monoclonal antibody and the results were quantitatively analyzed to measure the changes in PDGF-BB protein expression in the lung tissue. The results showed: (1) MP polymerase chain reaction (PCR) test showed positive results in the bronchoalveolar lavage fluid (BALF) from all of the MP-infected rats (infectious group, n=4), while they were all negative in BALF from the control group (n=4,P<0.05) and from those rats both infected with MP and, at the same time, treated with erythromycin (treating group n=4,P<0.05). Bacterial cultures of the bronchial and lung tissue were negative in all three groups. Using transmission electron microscope the widened interalveolar septa with increased amount of collagen were found in the infectious group, while there were no obvious abnormalities in the other two groups. (2) Strong positive stain of PDGF-BB protein was found in the interstitial conncetive tissue, the bronchial wall and the wall of blood vessels in the lung tissue from the infectious group. The integral optical density was 37.90±10.14,which was significantly higher than the value of control group (7.54±1.98,P<0.05) and the treating group (10.90±3.30,P<0.05). These results suggest that PDGF-BB protein expression is increased in the lung tissue with MP-infection, which may by involved in the process of the pathogenesis of pulmonary interstitial fibrosis caused by repeated MP-infection.