THE EFFECT OF ENCEPHALITOZOON INTESTINALIS ON OXIDATIVE STRESS AND CYTOKINE LEVELS IN U937 CELLS: AN IN VITRO STUDY

Journal of Applied Biological Sciences

article

Meryem Şentürk¹  Ülfet Çetinkaya²  Meryem Eren¹  Arzuv Charyyeva³ 

[1] Erciyes University, Faculty of Veterinary Medicine, Department of Biochemistry;Erciyes University Halil Bayraktar Vocational School of Health Services;Erciyes University, Faculty of Medicine, Department of Parasitology

关键词: Antioxidant;    cytokine;    Encephalitozoon intestinalis;    oxidative stress;    U937.;   

DOI  :  10.5281/zenodo.7579943

学科分类：生物科学（综合）

来源: Nobel Bilim ve Arasirma Merkezi/Nobel Science and Research Cente

【 摘 要 】

This in vitro study was performed to investigate the changes in nitric oxide (NO), malondialdehyde (MDA), total antioxidant capacity (TAC), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) levels in human monocytic (U937) cells infected with Encephalitozoon intestinalis. E. intestinalis was first cultured in the African green monkey renal epithelial (Vero) cells to obtain sufficient amount of parasite for the study. U937 human macrophage cell line and E. intestinalis 50506 (ATCC) strain were used in the study. U937 macrophages were infected with 5x106 spores after stimulation with Phorbol 12-Myristate 13-Acetate (PMA) and uninfected U937 cells were used as control. Culture media were collected at the 6th, 12th, and 24th hour after infection to determine NO, MDA, TAC, TNF-α and IL-10 levels. NO levels significantly increased at the 6 th, 12th and 24th hour. There was no significant difference in MDA and TAC levels at the 6th and 12th hour, but a significant increase in MDA, and a significant decrease in TAC was observed at the 24th hour. TNF-α levels did not differ in all sampling times, and IL10 level decreased only at the 6 th hour. In conclusion, E. intestinalis caused oxidative stress by increasing the levels of oxidants (NO and MDA) and by suppressing TAC level without no significant changes in cytokine levels in U937 cell line.

【 授权许可】

Unknown