国际医学寄生虫病杂志
國際醫學寄生蟲病雜誌
국제의학기생충병잡지
INTERNATIONAL JOURNAL OF MEDICAL PARASITIC DISEASES
2012年
3期
133-137
,共5页
刘现兵%赵明东%张海霞%姜昱竹%徐晓艳%张瑞金%刘杨%陈翠玲%胡雪梅
劉現兵%趙明東%張海霞%薑昱竹%徐曉豔%張瑞金%劉楊%陳翠玲%鬍雪梅
류현병%조명동%장해하%강욱죽%서효염%장서금%류양%진취령%호설매
刚地弓形虫RH株%血细胞%脾淋巴细胞%Crry%CD55
剛地弓形蟲RH株%血細胞%脾淋巴細胞%Crry%CD55
강지궁형충RH주%혈세포%비림파세포%Crry%CD55
Toxoplasma gondii RH strain%Hemocyte%Spleen lymphocyte%Crry%CD55
目的 探讨刚地弓形虫急性感染对小鼠外周血细胞和脾淋巴细胞表面补体调节蛋白Crry和CD55表达的影响.方法 将30只雄性C57BL/6小鼠按完全随机分组法分为感染组(20只)和对照组(10只).感染组小鼠每只腹腔注射1.0×104个RH株刚地弓形虫速殖子,对照组注射等量生理盐水.感染组依次于感染后2d和5d采集标本,同时对对照组取材.采用流式细胞仪检测小鼠外周血红细胞、白细胞及脾淋巴细胞Crry与CD55的表达情况.结果 ①感染后2d小鼠外周血红细胞Crry和CD55阳性表达率依次为(96.17±2.86)％和(65.23±4.99)％,对照组依次为(98.24±0.83)％和(68.57±5.31)％,组间差异均无有统计学意义；感染后5d,其红细胞Crry和CD55阳性率依次为(81.77±4.51)％、(51.72±8.29)％,对照组依次为(97.94±0.95)％、(70.57±6.44)％,感染组较对照组降低(t=7.786,t=4.433,P＜0.01).②感染后2d,白细胞Crry和CD55阳性率依次为(96.74±3.76)％、(71.80±6.74)％,对照组依次为(97.25±1.16)％、(74.84±3.87)％,两组比较均无有统计学意义的差异；感染后5d,其阳性率依次为(93.46±4.38)％、(59.67±6.37)％,对照组依次为(97.47±1.56)％、(75.10±4.58)％,感染组比对照组降低(t=2.585,t=4.792,P＜0.05,P＜0.01).③感染后2d,脾淋巴细胞Crry和CD55阳性率依次为(97.74±1.55)％和(66.58±2.67)％,对照组依次为(98.20±1.19)％和(69.98±4.62)％,两组比较均无有统计学意义的差异；感染5d后,其阳性率依次为(94.71±3.59)％、(56.86±6.98)％,对照组依次为(98.24±1.63)％、(71.18±4.09)％,其中,感染组CD55阳性率较对照组降低(t=4.195,P＜0.01),而Crry阳性率较对照组无有统计学意义的差异.结论 小鼠感染刚地弓形虫RH株后,不会立刻影响外周血和脾淋巴细胞补体调节蛋白Crry、CD55表达水平；随着病情发展,刚地弓形虫感染可导致机体免疫细胞补体调节蛋白的表达水平降低,但对不同免疫细胞各补体调节蛋白影响程度并不相同.
目的 探討剛地弓形蟲急性感染對小鼠外週血細胞和脾淋巴細胞錶麵補體調節蛋白Crry和CD55錶達的影響.方法 將30隻雄性C57BL/6小鼠按完全隨機分組法分為感染組(20隻)和對照組(10隻).感染組小鼠每隻腹腔註射1.0×104箇RH株剛地弓形蟲速殖子,對照組註射等量生理鹽水.感染組依次于感染後2d和5d採集標本,同時對對照組取材.採用流式細胞儀檢測小鼠外週血紅細胞、白細胞及脾淋巴細胞Crry與CD55的錶達情況.結果 ①感染後2d小鼠外週血紅細胞Crry和CD55暘性錶達率依次為(96.17±2.86)％和(65.23±4.99)％,對照組依次為(98.24±0.83)％和(68.57±5.31)％,組間差異均無有統計學意義；感染後5d,其紅細胞Crry和CD55暘性率依次為(81.77±4.51)％、(51.72±8.29)％,對照組依次為(97.94±0.95)％、(70.57±6.44)％,感染組較對照組降低(t=7.786,t=4.433,P＜0.01).②感染後2d,白細胞Crry和CD55暘性率依次為(96.74±3.76)％、(71.80±6.74)％,對照組依次為(97.25±1.16)％、(74.84±3.87)％,兩組比較均無有統計學意義的差異；感染後5d,其暘性率依次為(93.46±4.38)％、(59.67±6.37)％,對照組依次為(97.47±1.56)％、(75.10±4.58)％,感染組比對照組降低(t=2.585,t=4.792,P＜0.05,P＜0.01).③感染後2d,脾淋巴細胞Crry和CD55暘性率依次為(97.74±1.55)％和(66.58±2.67)％,對照組依次為(98.20±1.19)％和(69.98±4.62)％,兩組比較均無有統計學意義的差異；感染5d後,其暘性率依次為(94.71±3.59)％、(56.86±6.98)％,對照組依次為(98.24±1.63)％、(71.18±4.09)％,其中,感染組CD55暘性率較對照組降低(t=4.195,P＜0.01),而Crry暘性率較對照組無有統計學意義的差異.結論 小鼠感染剛地弓形蟲RH株後,不會立刻影響外週血和脾淋巴細胞補體調節蛋白Crry、CD55錶達水平；隨著病情髮展,剛地弓形蟲感染可導緻機體免疫細胞補體調節蛋白的錶達水平降低,但對不同免疫細胞各補體調節蛋白影響程度併不相同.
목적 탐토강지궁형충급성감염대소서외주혈세포화비림파세포표면보체조절단백Crry화CD55표체적영향.방법 장30지웅성C57BL/6소서안완전수궤분조법분위감염조(20지)화대조조(10지).감염조소서매지복강주사1.0×104개RH주강지궁형충속식자,대조조주사등량생리염수.감염조의차우감염후2d화5d채집표본,동시대대조조취재.채용류식세포의검측소서외주혈홍세포、백세포급비림파세포Crry여CD55적표체정황.결과 ①감염후2d소서외주혈홍세포Crry화CD55양성표체솔의차위(96.17±2.86)％화(65.23±4.99)％,대조조의차위(98.24±0.83)％화(68.57±5.31)％,조간차이균무유통계학의의；감염후5d,기홍세포Crry화CD55양성솔의차위(81.77±4.51)％、(51.72±8.29)％,대조조의차위(97.94±0.95)％、(70.57±6.44)％,감염조교대조조강저(t=7.786,t=4.433,P＜0.01).②감염후2d,백세포Crry화CD55양성솔의차위(96.74±3.76)％、(71.80±6.74)％,대조조의차위(97.25±1.16)％、(74.84±3.87)％,량조비교균무유통계학의의적차이；감염후5d,기양성솔의차위(93.46±4.38)％、(59.67±6.37)％,대조조의차위(97.47±1.56)％、(75.10±4.58)％,감염조비대조조강저(t=2.585,t=4.792,P＜0.05,P＜0.01).③감염후2d,비림파세포Crry화CD55양성솔의차위(97.74±1.55)％화(66.58±2.67)％,대조조의차위(98.20±1.19)％화(69.98±4.62)％,량조비교균무유통계학의의적차이；감염5d후,기양성솔의차위(94.71±3.59)％、(56.86±6.98)％,대조조의차위(98.24±1.63)％、(71.18±4.09)％,기중,감염조CD55양성솔교대조조강저(t=4.195,P＜0.01),이Crry양성솔교대조조무유통계학의의적차이.결론 소서감염강지궁형충RH주후,불회립각영향외주혈화비림파세포보체조절단백Crry、CD55표체수평；수착병정발전,강지궁형충감염가도치궤체면역세포보체조절단백적표체수평강저,단대불동면역세포각보체조절단백영향정도병불상동.
Objective To investigate the effect on Crry and CD55 in peripheral blood cell and spleen lymphocytes of C57BL/6 mice infected with Toxoplasma gondii (T.gondii).Methods Thirty male C57BL/6 mice were randomly divided into infected group (20mice) and control group (10mice).The mouse in infected group was intraperitoneally injected with 1.0×104 of living T.gondii RH strain tachyzoites while the mouse in the control group was injected with physiological saline.Specimens were acquired at 2d and 5d after injection.Crry and CD55 in peripheral blood cells and spleen lymphocytes were measured with flow cytometry.Results ①The positive percentages of Crry and CD55 on erythrocytes were (96.17±2.86)％,(65.23±4.99)％ in the infected group after 2d infection,and (98.24±0.83)％,(68.57±5.31)％ in the control group.There was no significant difference between two groups.After 5d,the positive percentages of Crry and CD55 were (81.77±4.51)％,(51.72±8.29)％ and (97.94±0.95)％,(70.57±6.44)％.Compared to control group,the positive percentages in the infected group were decreased significantly (t=7.786,t=4.433,P＜0.01).②The positive percentages of Crry and CD55 on leukocyte were (96.74±3.76)％,(71.80±6.74)％ in the infected group after 2d infection,and (97.25±1.16)％,(74.84±3.87)％ in the control group.There was no significant difference between two groups.After 5d,the positive percentages of Crry and CD55 were (93.464±4.38)％,(59.67±6.37)％ and (97.47±1.56)％,(75.10±4.58)％respectively in two groups.Compared to control group,the positive percentages in the infected group were decreased significantly (t=2.585,t=4.792,P＜0.05,P＜0.01).③The positive percentages of Crry and CD55 on spleen lymphocytes were (97.74±1.55)％,(66.58±2.67)％ in the infected group after 2d infection,and (98.20±1.19)％,(69.98±4.62)％ in the control group.There was no significant difference between two groups.After 5d,the positive percentages of Crry and CD55 were (94.71±3.59)％,(56.86±6.98)％ and (98.24±1.63)％,(71.18±4.09)％.Compared to control group,the positive percentages of CD55 in the infected group were decreased significantly(t=4.195,P＜0.01),but the positive percentages of Crry were not decreased notably.Conclusion The infection with T.gondii may not affect rapidly on the expression of complement regulatory proteins on peripheral blood cells and spleen lymphocytes.Along with development of infection,the positive percentages of Crry and CD55 were influenced by T.gondii RH strain at various levels.
