Background

Autophagy process is an important defense mechanism against intracellular infection. This process plays a critical role in limiting the development of Toxoplasma gondii. This study aimed to investigate the effects of T. gondii profilin and tachyzoites on the expression of autophagy genes.

Methods and results

PMA-activated THP-1 cell line was incubated with T. gondii profilin and tachyzoites for 6 h. After RNA extraction and cDNA synthesis, the expression of Atg5, Atg7, Atg12, and LC3b was evaluated using real-time PCR. The results revealed statistically significant downregulation of Atg5 for 1.43 (P-value = 0.0062) and 4.15 (P-value = 0.0178) folds after treatment with T. gondii profilin and tachyzoites, respectively. Similar to Atg 5, Atg 12 revealed a statistically significant downregulation for profilin (1.41 fold; P-value = 0.0047) and T. gondii tachyzoites (3.25 fold; P-value = 0.011). The expression of Atg7 elevated in both T. gondii profilin (2.083 fold; P-value = 0.0087) and tachyzoites (1.64 fold; P-value = 0.206). T. gondii profilin and tachyzoites downregulated (1.04 fold; P-value = 0.0028) and upregulated (twofold; P-value = 0.091) the expression of LC3b, respectively.

Conclusions

Our findings suggest that T. gondii and profilin may manipulate autophagy via preventing from the formation of Atg5-12-16L complex to facilitate replication of T. gondii and development of toxoplasmosis.

中文翻译：

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弓形虫 profilin 和速殖子 RH 菌株可能通过下调 Atg5 和 Atg12 以及上调 Atg7 来操纵自噬

 背景

自噬过程是抵抗细胞内感染的重要防御机制。这一过程在限制弓形虫的生长方面发挥着关键作用。本研究旨在探讨弓形虫profilin和速殖子对自噬基因表达的影响。

 方法和结果

PMA 激活的 THP-1 细胞系与弓形虫profilin 和速殖子一起孵育 6 小时。 RNA提取和cDNA合成后，使用实时PCR评估Atg5、Atg7、Atg12和LC3b的表达。结果显示，用刚地弓形虫profilin 和速殖子处理后，Atg5 分别下调 1.43 倍（ P值 = 0.0062）和 4.15 倍（ P值 = 0.0178），具有统计学意义。与 Atg 5 类似，Atg 12 显示 profilin（1.41 倍； P值 = 0.0047）和弓形虫速殖子（3.25 倍； P值 = 0.011）统计显着下调。 Atg7 在弓形虫profilin（2.083 倍； P值 = 0.0087）和速殖子（1.64 倍； P值 = 0.206）中的表达均升高。 T. gondii profilin 和 tachyzoites 分别下调（1.04 倍； P值 = 0.0028）和上调（两倍； P值 = 0.091）LC3b 的表达。

 结论

我们的研究结果表明，弓形虫和 profilin 可能通过阻止 Atg5-12-16L 复合物的形成来操纵自噬，以促进弓形虫的复制和弓形体病的发展。