中华肾脏病杂志
中華腎髒病雜誌
중화신장병잡지
2014年
2期
134-138
,共5页
尹仕伟%张莹%唐莎%邹丽云%高雪静%张晋宇%吴玉章%张静波
尹仕偉%張瑩%唐莎%鄒麗雲%高雪靜%張晉宇%吳玉章%張靜波
윤사위%장형%당사%추려운%고설정%장진우%오옥장%장정파
抗体,抗中性白细胞胞质%血管炎%分子模拟%局灶坏死性肾小球肾炎%白细胞介素-17
抗體,抗中性白細胞胞質%血管炎%分子模擬%跼竈壞死性腎小毬腎炎%白細胞介素-17
항체,항중성백세포포질%혈관염%분자모의%국조배사성신소구신염%백세포개소-17
Antibodies,antineutrophil cytoplasmic%Vasculitis%Molecular mimicry%Focal necrotizing glomerulonephritis%Interleukin-17
目的 探讨细菌FimH融合蛋白诱导大鼠肾小球局灶坏死性损伤的可能机制.方法 采用纯化的大肠杆菌FimH1-156融合蛋白(150 μg)联合Titermax金佐剂(150μl)皮下注射免疫Wistar-Kyoto (WKY)大鼠,对照组采用PBS(150μl)联合Titermax金佐剂(150μl).监测各时间点(0、3、7、14、21、28、35、50 d)大鼠24 h尿蛋白量(mg)的变化,于免疫后21 d、35 d和50 d处死大鼠,检测大鼠血清BUN、Scr、尿酸(UA)水平,观察肾、肺组织病理变化,ELISA法检测血清白细胞介素(IL)-17A水平.结果 (1)模型组大鼠24 h尿蛋白量在免疫后第3天开始升高,第7、35、50天时显著高于对照组[(8.59±1.25) mg比(3.08±1.08) mg、(10.33±1.10) mg比(6.40±0.61)mg、(12.45±1.73) mg比(5.93±0.83) mg,均P＜0.05].(2)免疫后50 d,模型组大鼠血清BUN、Scr、UA水平均显著高于对照组[(6.76±0.20) mmol/L比(5.82±0.13) mmol/L、(58.00±1.53) μmol/L比(25.67±1.45) μmol/L、(61.67±7.27) μmol/L比(31.33±2.73) μmol/L,均P＜0.05].(3)免疫后35 d,肾脏组织显示局灶坏死,肺泡壁增厚、部分断裂及炎性细胞浸润,免疫后50 d肾小球新月体形成.(4)免疫WKY大鼠35、50 d后,模型组血清IL-17A水平均显著高于对照组[(46.97±5.00) ng/L比(1127±2.67) ng/L、(41.95±5.51)ng/L比(16.31±1.64) ng/L,均P＜0.05].(5)线性回归分析显示模型组大鼠血清IL-17A与24 h尿蛋白量呈正相关(r=0.557,P=0.021).结论 细菌FimH融合蛋白诱导大鼠肾小球局灶坏死性损伤及肺损伤,IL-17A参与了FimH融合蛋白诱导的大鼠肺、肾损伤过程.
目的 探討細菌FimH融閤蛋白誘導大鼠腎小毬跼竈壞死性損傷的可能機製.方法 採用純化的大腸桿菌FimH1-156融閤蛋白(150 μg)聯閤Titermax金佐劑(150μl)皮下註射免疫Wistar-Kyoto (WKY)大鼠,對照組採用PBS(150μl)聯閤Titermax金佐劑(150μl).鑑測各時間點(0、3、7、14、21、28、35、50 d)大鼠24 h尿蛋白量(mg)的變化,于免疫後21 d、35 d和50 d處死大鼠,檢測大鼠血清BUN、Scr、尿痠(UA)水平,觀察腎、肺組織病理變化,ELISA法檢測血清白細胞介素(IL)-17A水平.結果 (1)模型組大鼠24 h尿蛋白量在免疫後第3天開始升高,第7、35、50天時顯著高于對照組[(8.59±1.25) mg比(3.08±1.08) mg、(10.33±1.10) mg比(6.40±0.61)mg、(12.45±1.73) mg比(5.93±0.83) mg,均P＜0.05].(2)免疫後50 d,模型組大鼠血清BUN、Scr、UA水平均顯著高于對照組[(6.76±0.20) mmol/L比(5.82±0.13) mmol/L、(58.00±1.53) μmol/L比(25.67±1.45) μmol/L、(61.67±7.27) μmol/L比(31.33±2.73) μmol/L,均P＜0.05].(3)免疫後35 d,腎髒組織顯示跼竈壞死,肺泡壁增厚、部分斷裂及炎性細胞浸潤,免疫後50 d腎小毬新月體形成.(4)免疫WKY大鼠35、50 d後,模型組血清IL-17A水平均顯著高于對照組[(46.97±5.00) ng/L比(1127±2.67) ng/L、(41.95±5.51)ng/L比(16.31±1.64) ng/L,均P＜0.05].(5)線性迴歸分析顯示模型組大鼠血清IL-17A與24 h尿蛋白量呈正相關(r=0.557,P=0.021).結論 細菌FimH融閤蛋白誘導大鼠腎小毬跼竈壞死性損傷及肺損傷,IL-17A參與瞭FimH融閤蛋白誘導的大鼠肺、腎損傷過程.
목적 탐토세균FimH융합단백유도대서신소구국조배사성손상적가능궤제.방법 채용순화적대장간균FimH1-156융합단백(150 μg)연합Titermax금좌제(150μl)피하주사면역Wistar-Kyoto (WKY)대서,대조조채용PBS(150μl)연합Titermax금좌제(150μl).감측각시간점(0、3、7、14、21、28、35、50 d)대서24 h뇨단백량(mg)적변화,우면역후21 d、35 d화50 d처사대서,검측대서혈청BUN、Scr、뇨산(UA)수평,관찰신、폐조직병리변화,ELISA법검측혈청백세포개소(IL)-17A수평.결과 (1)모형조대서24 h뇨단백량재면역후제3천개시승고,제7、35、50천시현저고우대조조[(8.59±1.25) mg비(3.08±1.08) mg、(10.33±1.10) mg비(6.40±0.61)mg、(12.45±1.73) mg비(5.93±0.83) mg,균P＜0.05].(2)면역후50 d,모형조대서혈청BUN、Scr、UA수평균현저고우대조조[(6.76±0.20) mmol/L비(5.82±0.13) mmol/L、(58.00±1.53) μmol/L비(25.67±1.45) μmol/L、(61.67±7.27) μmol/L비(31.33±2.73) μmol/L,균P＜0.05].(3)면역후35 d,신장조직현시국조배사,폐포벽증후、부분단렬급염성세포침윤,면역후50 d신소구신월체형성.(4)면역WKY대서35、50 d후,모형조혈청IL-17A수평균현저고우대조조[(46.97±5.00) ng/L비(1127±2.67) ng/L、(41.95±5.51)ng/L비(16.31±1.64) ng/L,균P＜0.05].(5)선성회귀분석현시모형조대서혈청IL-17A여24 h뇨단백량정정상관(r=0.557,P=0.021).결론 세균FimH융합단백유도대서신소구국조배사성손상급폐손상,IL-17A삼여료FimH융합단백유도적대서폐、신손상과정.
Objective To investigate the mechanism of focal necrotizing glomerulonephritis induced by FimH fusion protein.Methods Wistar-Kyoto (WKY) rats were immunized with purified FimH fusion protein (150 μg) emulsified in Titermax Gold.Controls received PBS in Titermax Gold alone.Glomerular injuries were assessed by 24-hour urinary protein,urea nitrogen (BUN),serum creatinine (Scr),serum uric acid (UA) and histomorphology.The levels of intedeukin-17A (IL-17A)were detected by ELISA assay.Results The levels of 24-hour urinary protein began to rise at 3rd day after immunization with FimH fusion protein,and were significantly higher than control group on 7th,35th and 50th day [(8.59±1.25) mg vs (3.08±1.08) mg,(10.33±1.10) mg vs (6.40±0.61) mg,(12.45±1.73)mg vs (5.93±0.83) mg,all P ＜ 0.05].The serum levels of BUN,Scr,UA in model rats were increased significantly at 50th day [(6.76±0.20) mmol/L vs (5.82±0.13) mmol/L,(58.00±1.53) μmol/L vs (25.67± 1.45) μmol/L,(61.67±7.27) μmol/L vs (31.33±2.73) μmol/L,all P＜ 0.05] compared to control group.WKY rats immunized with FimH fusion protein showed segmental necrosis of glomerular capillaries,alveolar wall thickening,and significant inflammatory cells infiltration on 35 th day,and glomerular crescent formation after 50 days.The serum levels of IL-17A were increased significantly compared to control group on 35th and 504 day [(46.97±5.00) ng/L vs (11.27±2.67) ng/L,(41.95±5.51) ng/L vs (16.31± 1.64) ng/L,P ＜ 0.05].The IL-17A level was positively correlated with 24-hour urinary protein in model group (r=0.557,P=0.021).Cornclusion Bacteria FimH protein can induce glomerular focal necrotic lesion and lung injury in WKY rats,and IL-17A may involve in the damage process.
