微生物学杂志
微生物學雜誌
미생물학잡지
JOURNAL OF MICROBIOLOGY
2013年
6期
70-74
,共5页
陈凡%张宁洁%余平%程文
陳凡%張寧潔%餘平%程文
진범%장저길%여평%정문
沙眼衣原体%生殖道感染%促炎性细胞因子
沙眼衣原體%生殖道感染%促炎性細胞因子
사안의원체%생식도감염%촉염성세포인자
Chlamydia trachomatis%genital infection%inflammatory promotive cytokine
建立小鼠生殖道沙眼衣原体感染模型,观察小鼠生殖道局部促炎性细胞因子的表达。将小鼠生物型沙眼衣原体C. muridarum 1×104 IFU阴道接种于C57B6背景雌性小鼠,取感染后阴道拭子做沙眼衣原体培养,计算IFU,监测小鼠感染和病原体清除情况;80 d后处死小鼠,检测子宫输卵管病理改变;ELISA检测感染过程中小鼠生殖道促炎性细胞因子IL-1α、IL-6、MIP-2和TNF-α产生情况。小鼠感染在第3至第15天维持较高水平,然后病原体被逐渐清除,整个病程约3~5周;病理检测显示子宫输卵有严重炎症、管腔扩张积水,狭窄等;于感染后第3天检测到局部IL-1α、IL-6、MIP-2分泌,第7天达高峰,然后逐渐下降至正常水平( IL-6于11 d恢复正常,IL-1α和 MIP-2于15 d恢复正常)。 TNF-α仅在第7天检测到高水平表达。相对于TNF-α和IL-6,IL-1α和MIP-2维持时间较长。成功建立沙眼衣原体感染小鼠生殖道模型,沙眼衣原体急性感染可诱导小鼠生殖道局部分泌IL-1α、IL-6、MIP-2和TNF-α。
建立小鼠生殖道沙眼衣原體感染模型,觀察小鼠生殖道跼部促炎性細胞因子的錶達。將小鼠生物型沙眼衣原體C. muridarum 1×104 IFU陰道接種于C57B6揹景雌性小鼠,取感染後陰道拭子做沙眼衣原體培養,計算IFU,鑑測小鼠感染和病原體清除情況;80 d後處死小鼠,檢測子宮輸卵管病理改變;ELISA檢測感染過程中小鼠生殖道促炎性細胞因子IL-1α、IL-6、MIP-2和TNF-α產生情況。小鼠感染在第3至第15天維持較高水平,然後病原體被逐漸清除,整箇病程約3~5週;病理檢測顯示子宮輸卵有嚴重炎癥、管腔擴張積水,狹窄等;于感染後第3天檢測到跼部IL-1α、IL-6、MIP-2分泌,第7天達高峰,然後逐漸下降至正常水平( IL-6于11 d恢複正常,IL-1α和 MIP-2于15 d恢複正常)。 TNF-α僅在第7天檢測到高水平錶達。相對于TNF-α和IL-6,IL-1α和MIP-2維持時間較長。成功建立沙眼衣原體感染小鼠生殖道模型,沙眼衣原體急性感染可誘導小鼠生殖道跼部分泌IL-1α、IL-6、MIP-2和TNF-α。
건립소서생식도사안의원체감염모형,관찰소서생식도국부촉염성세포인자적표체。장소서생물형사안의원체C. muridarum 1×104 IFU음도접충우C57B6배경자성소서,취감염후음도식자주사안의원체배양,계산IFU,감측소서감염화병원체청제정황;80 d후처사소서,검측자궁수란관병리개변;ELISA검측감염과정중소서생식도촉염성세포인자IL-1α、IL-6、MIP-2화TNF-α산생정황。소서감염재제3지제15천유지교고수평,연후병원체피축점청제,정개병정약3~5주;병리검측현시자궁수란유엄중염증、관강확장적수,협착등;우감염후제3천검측도국부IL-1α、IL-6、MIP-2분비,제7천체고봉,연후축점하강지정상수평( IL-6우11 d회복정상,IL-1α화 MIP-2우15 d회복정상)。 TNF-α부재제7천검측도고수평표체。상대우TNF-α화IL-6,IL-1α화MIP-2유지시간교장。성공건립사안의원체감염소서생식도모형,사안의원체급성감염가유도소서생식도국부분비IL-1α、IL-6、MIP-2화TNF-α。
Model of mouse genital tract infected by C. trachomatis was established to observe the expression of in-flammatory promotive cytokines in mice genital tract. Female mice of C57B6 background were inoculation with C. tra-chomatis biotype mouse intravaginally at 1í104 IFU. The swabs were then collected from mice vaginal tracts and cul-tured for C. trachomatis and calculated the IFU to monitor the situation of the infection and the removal of the patho-gen in mice. 80 days after the infection the mice were killed and tested for pathological changes in their wombs and oviducts. Tested for their production of inflammatory promotive cytokines IL-1α, IL-6, MIP-2, and TNF-α with ELISA determination during the infection process. The results showed that at day 3 through day 15 the infection was maintained at fairly high level, then the pathogen was gradually removed, the course of the disease was about 3~5 weeks;the pathogenic tests showed that the oviduct had serious inflammation, and the uterus cavity was seriously di-lated and had serious hydrops and stenosis etc. The early local secretion of IL-1α, IL-6 and MIP-2 could be detected on day 3 after the infection, then rise to the highest level at day 7, and gradually decreased to normal level on day 11 (IL-6) and day 15 (IL-1αand MIP-2). TNF-αcould be detected only on day 7 with a high level. As compared with TNF-αand IL-6, IL-1αand MIP-2 maintained for a longer time. The establishment of model of C. trachomatis to in-fect mouse genital tract was successful, C. trachomatis acute infection could induce mouse genital tract to excrete lo-cally IL-1α, IL-6, MIP-2 and TNF-α.