Journalartikel

Besnoitia besnoiti-driven endothelial host cell cycle alteration


AutorenlisteVelasquez, Zahady D.; Lopez-Osorio, Sara; Pervizaj-Oruqaj, Learta; Herold, Susanne; Hermosilla, Carlos; Taubert, Anja

Jahr der Veröffentlichung2020

Seiten2563-2577

ZeitschriftParasitology Research

Bandnummer119

Heftnummer8

ISSN0932-0113

eISSN1432-1955

Open Access StatusHybrid

DOI Linkhttps://doi.org/10.1007/s00436-020-06744-x

VerlagSpringer


Abstract
Besnoitia besnoitiis 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 parasiteToxoplasma gondii,B. besnoitihas 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 thatT. gondiitachyzoites 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 forB. besnoitiinfections. The current data showed that-in terms of host cell cycle modulation-infections of BUVEC byB. besnoititachyzoites indeed differ significantly from those byT. gondii. As such, cyclin expression patterns demonstrated a significant upregulation of cyclin E1 inB. 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 respectiveT. gondii-related data, we furthermore found a significant upregulation of histone H3 (S10) phosphorylation inB. 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 byB. besnoitisince infected cells showed increased nuclear PCNA levels when compared with that of control cells.



Zitierstile

Harvard-ZitierstilVelasquez, Z., Lopez-Osorio, S., Pervizaj-Oruqaj, L., Herold, S., Hermosilla, C. and Taubert, A. (2020) Besnoitia besnoiti-driven endothelial host cell cycle alteration, Parasitology Research, 119(8), pp. 2563-2577. https://doi.org/10.1007/s00436-020-06744-x

APA-ZitierstilVelasquez, Z., Lopez-Osorio, S., Pervizaj-Oruqaj, L., Herold, S., Hermosilla, C., & Taubert, A. (2020). Besnoitia besnoiti-driven endothelial host cell cycle alteration. Parasitology Research. 119(8), 2563-2577. https://doi.org/10.1007/s00436-020-06744-x



Schlagwörter


Apicomplexan parasitesCOCCIDIAFORCE GENERATIONHISTONE H3 PHOSPHORYLATIONHistone H3 S10S-PHASESUBUNITTOXOPLASMA-GONDII


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