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Abstract：
BACKGROUND: Toxoplasma gondii is an intracellular protozoan parasite that is widely distributed in humans and warm-blooded animals. T. gondii chronic infections can cause toxoplasmic encephalopathy, adverse pregnancy, and male reproductive disorders. In male reproduction, the main function of the testis is to provide a stable place for spermatogenesis and immunological protection. The disorders affecting testis tissue encompass abnormalities in the germ cell cycle, spermatogenic retardation, or complete cessation of sperm development. However, the mechanisms of interaction between T. gondii and the reproductive system is unclear. The aims were to study the expression levels of genes related to spermatogenesis, following T. gondii infection, in mouse testicular tissue.
METHODS: RNA-seq sequencing was carried out on mouse testicular tissues from mice infected or uninfected with the T. gondii type II Prugniaud (PRU) strain and validated in combination with real-time quantitative PCR and immunofluorescence assays.
RESULTS: The results showed that there were 250 significant differentially expressed genes (DEGs) (P < 0.05, |log2fold change| ≧ 1). Bioinformatics analysis showed that 101 DEGs were annotated to the 1696 gene ontology (GO) term. While there was a higher number of DEGs in the biological process classification as a whole, the GO enrichment revealed a significant presence of DEGs in the cellular component classification. The Arhgap18 and Syne1 genes undergo regulatory changes following T. gondii infection, and both were involved in shaping the cytoskeleton of the blood-testis barrier (BTB). The number of DEGs enriched in the MAPK signaling pathway, the ERK1/2 signaling pathway, and the JNK signaling pathway were significant. The PTGDS gene is located in the Arachidonic acid metabolism pathway, which plays an important role in the formation and maintenance of BTB in the testis. The expression of PTGDS is downregulated subsequent to T. gondii infection, potentially exerting deleterious effects on the integrity of the BTB and the spermatogenic microenvironment within the testes.
CONCLUSIONS: Overall, our research provides in-depth insights into how chronic T. gondii infection might affect testicular tissue and potentially impact male fertility. These findings offer a new perspective on the impact of T. gondii infection on the male reproductive system.
METHODS: RNA-seq sequencing was carried out on mouse testicular tissues from mice infected or uninfected with the T. gondii type II Prugniaud (PRU) strain and validated in combination with real-time quantitative PCR and immunofluorescence assays.
RESULTS: The results showed that there were 250 significant differentially expressed genes (DEGs) (P < 0.05, |log2fold change| ≧ 1). Bioinformatics analysis showed that 101 DEGs were annotated to the 1696 gene ontology (GO) term. While there was a higher number of DEGs in the biological process classification as a whole, the GO enrichment revealed a significant presence of DEGs in the cellular component classification. The Arhgap18 and Syne1 genes undergo regulatory changes following T. gondii infection, and both were involved in shaping the cytoskeleton of the blood-testis barrier (BTB). The number of DEGs enriched in the MAPK signaling pathway, the ERK1/2 signaling pathway, and the JNK signaling pathway were significant. The PTGDS gene is located in the Arachidonic acid metabolism pathway, which plays an important role in the formation and maintenance of BTB in the testis. The expression of PTGDS is downregulated subsequent to T. gondii infection, potentially exerting deleterious effects on the integrity of the BTB and the spermatogenic microenvironment within the testes.
CONCLUSIONS: Overall, our research provides in-depth insights into how chronic T. gondii infection might affect testicular tissue and potentially impact male fertility. These findings offer a new perspective on the impact of T. gondii infection on the male reproductive system.
摘要：
背景：弓形虫是一种细胞内原生动物寄生虫，广泛分布于人类和温血动物中。弓形虫慢性感染可引起弓形虫脑病，不良妊娠，和男性生殖障碍。在男性繁殖中，睾丸的主要功能是为精子发生和免疫保护提供稳定的场所。影响睾丸组织的疾病包括生殖细胞周期的异常，生精迟缓,或完全停止精子发育。然而,弓形虫与生殖系统相互作用的机制尚不清楚。目的是研究精子发生相关基因的表达水平,弓形虫感染后,在小鼠睾丸组织中。
方法：对感染或未感染弓形虫II型Prugniaud（PRU）菌株的小鼠睾丸组织进行RNA-seq测序，并结合实时定量PCR和免疫荧光分析进行验证。
结果：结果表明，有250个显着的差异表达基因（DEGs）（P<0.05，|log2倍变化|≥1）。生物信息学剖析显示，101DEGs注释为1696基因本体论(GO)术语。虽然整个生物过程分类中的DEGs数量较多，GO富集显示DEGs在细胞组分分类中的显著存在。弓形虫感染后，Arhgap18和Syne1基因发生调节变化，两者都参与了形成血睾丸屏障（BTB）的细胞骨架。MAPK信号通路中富含DEGs的数量,ERK1/2信号通路，和JNK信号通路显著。PTGDS基因位于花生四烯酸代谢通路,在睾丸中BTB的形成和维持中起着重要作用。弓形虫感染后，PTGDS的表达下调，可能对睾丸内BTB的完整性和生精微环境产生有害影响。
结论：总体而言，我们的研究深入了解了慢性弓形虫感染可能如何影响睾丸组织并可能影响男性生育能力.这些发现为弓形虫感染对男性生殖系统的影响提供了新的视角。
方法：对感染或未感染弓形虫II型Prugniaud（PRU）菌株的小鼠睾丸组织进行RNA-seq测序，并结合实时定量PCR和免疫荧光分析进行验证。
结果：结果表明，有250个显着的差异表达基因（DEGs）（P<0.05，|log2倍变化|≥1）。生物信息学剖析显示，101DEGs注释为1696基因本体论(GO)术语。虽然整个生物过程分类中的DEGs数量较多，GO富集显示DEGs在细胞组分分类中的显著存在。弓形虫感染后，Arhgap18和Syne1基因发生调节变化，两者都参与了形成血睾丸屏障（BTB）的细胞骨架。MAPK信号通路中富含DEGs的数量,ERK1/2信号通路，和JNK信号通路显著。PTGDS基因位于花生四烯酸代谢通路,在睾丸中BTB的形成和维持中起着重要作用。弓形虫感染后，PTGDS的表达下调，可能对睾丸内BTB的完整性和生精微环境产生有害影响。
结论：总体而言，我们的研究深入了解了慢性弓形虫感染可能如何影响睾丸组织并可能影响男性生育能力.这些发现为弓形虫感染对男性生殖系统的影响提供了新的视角。
