Background

Toxocara canis, a source of visceral larva migrans, causes toxocariasis and induces respiratory symptoms. The reasons by which the pulmonary pathological alteration in the lungs infected with T. canis remain unclear.

Methods

The involvement of the pulmonary pathological alteration by histology, enzyme activity, and Western blot analysis in the lungs of BALB/c mice after the infection of 2000 embryonated eggs.

Results

The pathological effects gradually increased after the infection culminated in severe leukocyte infiltration and hemorrhage from days 4–14 post-inoculation. Gelatin zymography using substrate showed that the relative activity of matrix metalloproteinase (MMP) −9 and MMP-2 significantly increased in T. canis-infected mice. Western blot analysis indicated that the MMPs protein level of fibronectin monomer significantly increased in T. canis-infected mice compared with that in uninfected control. T. canis larvae mainly initiated leukocyte infiltration and hemorrhage in the lungs.

Conclusion

These phenomena subsequently induced the activities of MMPs in parallel with the pathological changes in early stage pulmonary inflammation. In conclusion, T. canis larval migration activated the MMPs and caused pulmonary pathogenesis.

中文翻译：

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犬弓蛔虫诱导的肺部发病机制中的基质金属蛋白酶激活

背景

犬弓蛔虫是内脏幼虫移行的来源，会引起弓蛔虫病并诱发呼吸道症状。T. canis感染肺部肺部病理改变的原因尚不清楚。

方法

BALB/c 小鼠在感染 2000 个胚胎后肺部的组织学、酶活性和蛋白质印迹分析涉及肺部病理改变。

结果

感染在接种后第4-14天达到严重的白细胞浸润和出血后，病理作用逐渐增加。使用底物的明胶酶谱显示基质金属蛋白酶 (MMP) -9 和 MMP-2 的相对活性在T. canis感染的小鼠中显着增加。Western印迹分析表明，与未感染的对照相比，T. canis感染的小鼠中纤连蛋白单体的MMPs蛋白水平显着增加。T. canis幼虫主要引发肺部白细胞浸润和出血。

结论

这些现象随后诱导 MMPs 的活性与早期肺部炎症的病理变化平行。总之，T. canis幼虫迁移激活了 MMPs 并引起了肺部发病机制。