Besnoitia besnoiti is an important obligate intracellular parasite of cattle which primarily infects host endothelial cells of blood vessels during the acute phase of infection. Similar to the closely related parasite Toxoplasma gondii, B. besnoiti has fast proliferating properties leading to rapid host cell lysis within 24–30 h p.i. in vitro. Some apicomplexan parasites were demonstrated to modulate the host cellular cell cycle to successfully perform their intracellular development. As such, we recently demonstrated that T. gondii tachyzoites induce G2/M arrest accompanied by chromosome missegregation, cell spindle alteration, formation of supernumerary centrosomes, and cytokinesis impairment when infecting primary bovine umbilical vein endothelial cells (BUVEC). Here, we follow a comparative approach by using the same host endothelial cell system for B. besnoiti infections. The current data showed that—in terms of host cell cycle modulation—infections of BUVEC by B. besnoiti tachyzoites indeed differ significantly from those by T. gondii. As such, cyclin expression patterns demonstrated a significant upregulation of cyclin E1 in B. besnoiti–infected BUVEC, thereby indicating parasite-driven host cell stasis at G1-to-S phase transition. In line, the mitotic phase of host cell cycle was not influenced since alterations of chromosome segregation, mitotic spindle formation, and cytokinesis were not observed. In contrast to respective T. gondii–related data, we furthermore found a significant upregulation of histone H3 (S10) phosphorylation in B. besnoiti–infected BUVEC, thereby indicating enhanced chromosome condensation to occur in these cells. In line to altered G1/S-transition, we here additionally showed that subcellular abundance of proliferating cell nuclear antigen (PCNA), a marker for G1 and S phase sub-stages, was affected by B. besnoiti since infected cells showed increased nuclear PCNA levels when compared with that of control cells.

贝氏疟原虫是牛的一种重要的专性细胞内寄生虫，在感染的急性期主要感染宿主的血管内皮细胞。与紧密相关的寄生虫弓形虫相似，B。besnoiti具有快速增殖的特性，可在体外pi 24-30 h内快速裂解宿主细胞。已证明一些apicomplexan寄生虫可以调节宿主细胞的细胞周期，从而成功地完成其细胞内发育。因此，我们最近证明了弓形虫速殖子感染原发性牛脐静脉内皮细胞（BUVEC）时，会导致G2 / M停滞，并伴随染色体错集，细胞纺锤体改变，多余的中心体的形成和胞质分裂障碍。在这里，我们遵循一种比较方法，将同一宿主内皮细胞系统用于贝氏芽孢杆菌感染。当前数据表明，就宿主细胞周期调控而言，贝氏芽孢杆菌速殖子对BUVEC的感染确实与弓形虫的感染明显不同。因此，细胞周期蛋白的表达模式表明，B。besnoiti –中的细胞周期蛋白E1明显上调。感染BUVEC，从而表明在G1到S的相变过程中由寄生虫驱动的宿主细胞停滞。一致地，宿主细胞周期的有丝分裂期不受影响，因为未观察到染色体分离，有丝分裂纺锤体形成和胞质分裂的改变。与各个弓形虫相关的数据相比，我们还发现在被贝氏芽孢杆菌感染的BUVEC中组蛋白H3（S10）磷酸化显着上调，从而表明这些细胞中染色体凝集的增强。与改变的G1 / S转变一致，我们在这里还显示，B。besnoiti影响了增殖细胞核抗原（PCNA）（G1和S期亚阶段的标志物）的亚细胞丰度 因为与对照细胞相比，受感染的细胞显示出增加的核PCNA水平。