中华皮肤科杂志 ›› 2009, Vol. 42 ›› Issue (8): 541-544.

• 论著 • 上一篇    下一篇

小鼠皮肤卡氏支孢霉感染动物模型的构建

柴宝1,吕桂霞2,沈永年2,陈伟2,刘维达2   

  1. 1. 广东省深圳市第六人民医院,暨深圳市南山区人民医院,广东医学院附属南山医院
    2. 南京 中国医学科学院北京协和医学院皮肤病研究所
  • 收稿日期:2009-04-16 修回日期:2009-04-22 出版日期:2009-08-15 发布日期:2009-08-10
  • 通讯作者: 柴宝

Establishment of a murine model for infection by Cladosporium carrionii

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  • Received:2009-04-16 Revised:2009-04-22 Online:2009-08-15 Published:2009-08-10

摘要:

目的 构建卡氏支孢霉感染小鼠模型。方法 ICR小鼠分为4组,A 组为健康小鼠,足垫皮下接种1 × 108孢子数/mL卡氏支孢霉悬液组;B组为免疫抑制小鼠,足垫皮下接种1 × 108孢子数/mL卡氏支孢霉悬液组;C组为免疫抑制小鼠足垫皮下接种1 × 106孢子数/mL卡氏支孢霉悬液组; D组为对照组,健康小鼠足垫皮下接种生理氯化钠溶液。接种后第7、30、60天时测量各组小鼠足垫厚度,处死并进行足垫病理及真菌检查。结果 A、B、C组小鼠接种处均出现肿胀、发黑、溃疡、结痂,感染发病率均为100%。A组足垫厚度在接种后第7天、30天分别为(2.85 ± 0.47) mm、(2.40 ± 0.45) mm,后者较前者显著下降(P < 0.05);第60天为(1.64 ± 0.13) mm,较第30天显著下降(P < 0.05)。B组在接种后第7天、30天分别为(1.80 ± 0.21) mm、(2.19 ± 0.27) mm,后者较前者显著增厚(P < 0.05);第60天为(1.86 ± 0.22) mm,较第30天显著下降(P < 0.05)。C组在接种后第7天、30天分别为(1.51 ± 0.11) mm、(1.98 ± 0.06) mm,后者较前者显著增厚(P < 0.05),第60天为(1.82 ± 0.09) mm,较第30天显著下降(P < 0.05)。D组则无显著改变(P > 0.05)。实验组基本病理改变为坏死、脓肿、慢性肉芽肿形成。HE、PAS染色可见硬壳小体,皮损处脓液直接镜检可见硬壳小体,培养为卡氏支孢霉生长。对照组未感染卡氏支孢霉。结论 卡氏支孢霉鼠足垫皮下接种免疫抑制和健康小鼠均可成功建立皮下着色真菌病模型。

Abstract:

Objective To develop a murine model for infection by Cladosporium carrioni. Methods A total of 72 ICR mice were equally divided into 4 groups, group A (healthy mice inoculated by C. carrioni suspension of 1 × 108 cfu conidia mL-1), group B (immuno-suppressed mice inoculated by C. carrioni suspension of 1 × 108 cfu conidia mL-1), group C (immuno-suppressed mice inoculated by C. carrioni suspension of 1 × 106 cfu conidia mL-1), group D (healthy mice inoculated by sodium chloride solution). C. carrioni suspension or sodium chloride solution was subcutaneously inoculated into foot pads of mice. On day 7, 30 and 60 after inoculation, 6 mice were killed in each group followed by the measurement of thickness of foot pads, pathology and mycology of skin samples taken from foot pads. Results In group A, B and C, there were swelling, blackening, ulceration and crusts at the inoculation site of all mice, with a morbidity of 100%. The thickness of foot pads in group A on day 30 was significantly higher than that on day 7 (2.40 ± 0.45 mm vs 2.85 ± 0.47 mm, P < 0.05), but lower than that on day 60 (1.64 ± 0.13 mm, P < 0.05). In group B, increased thickness of foot pads was observed on day 30 compared with that on day 7 and day 60 (2.19 ± 0.27 mm vs 1.80 ± 0.21 mm and 1.86 ± 0.22 mm, respectively, both P < 0.05), which was the case with group C (1.98 ± 0.06 mm vs 1.51 ± 0.11 mm and 1.82 ± 0.09 mm, respectively, both P < 0.05). No significant changes occurred to the thickness of foot pads in group D from day 7 to day 60 (P > 0.05). Pathological changes in group A, B and C included necrosis, abscess and chronic granuloma formation; dark brown sclerotic bodies were observed on HE and PAS staining as well as on direct microscopy; cultures of tissue samples grew Cladosporium carrionii. The mice in group D remained uninfected. Conclusion Mouse model for chromoblastomycosis may be established by subcutaneous inoculation of Cladosporium carrionii suspension into foot pads of healthy or immuno-suppressed mice.