Hepatitis E Virus Mediates Renal Injury via the Interaction between the Immune Cells and Renal Epithelium

Vaccines

Sara Adel¹  MohamedIsmail Seddik²  Asmaa Osman²  Lobna Abdel-Wahid³  EssamM. Abdel Aziz⁴  Eman Radwan⁵  MohamedA. El-Mokhtar⁶  IbrahimM. Sayed⁶  SaharA. Mandour⁷  MohamedA. Zarzour⁸  Nasreldin Mohammed⁸ 

[1] Department of Clinical Pathology, Faculty of Medicine, Al-Azhar University, Assiut 71515, Egypt;Department of Clinical Pathology, Faculty of Medicine, Assiut University, Assiut 71515, Egypt;Department of Internal Medicine, Faculty of Medicine, Assiut University, Assiut 71515, Egypt;Department of Internal Medicine, Nephrology Division, Faculty of Medicine, Assiut University, Assiut 71515, Egypt;Department of Medical Biochemistry, Faculty of Medicine, Assiut University, Assiut 71515, Egypt;Department of Medical Microbiology and Immunology, Faculty of Medicine, Assiut University, Assiut 71515, Egypt;Department of Microbiology and Immunology, Faculty of Pharmacy, Deraya University, Minia 66111, Egypt;Department of Urology and Renal Transplantation Centre, Faculty of Medicine, Assiut University Hospital, Assiut 71515, Egypt;

关键词: HEV;    renal disorder;    immune-mediated;    proximal tubular;    inflammatory cytokines;    chemokines;   

DOI  :  10.3390/vaccines8030454

来源: DOAJ

【 摘 要 】

Renal disorders are associated with Hepatitis E virus (HEV) infection. Progression to end-stage renal disease and acute kidney injury are complications associated with HEV infection. The mechanisms by which HEV mediates the glomerular diseases remain unclear. CD10⁺/CD13⁺ primary proximal tubular (PT) epithelial cells, isolated from healthy donors, were infected with HEV. Inflammatory markers and kidney injury markers were assessed in the presence or absence of peripheral blood mononuclear cells (PBMCs) isolated from the same donors. HEV replicated efficiently in the PT cells as shown by the increase in HEV load over time and the expression of capsid Ag. In the absence of PBMCs, HEV was not nephrotoxic, with no direct effect on the transcription of chemokines (Cxcl-9, Cxcl-10, and Cxcl-11) nor the kidney injury markers (kidney injury molecule 1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and interleukin 18 (lL-18)). While higher inflammatory responses, upregulation of chemokines and kidney injury markers expression, and signs of nephrotoxicity were recorded in HEV-infected PT cells cocultured with PBMCs. Interestingly, a significantly higher level of IFN-γ was released in the PBMCs-PT coculture compared to PT alone during HEV infection. In conclusion: The crosstalk between immune cells and renal epithelium and the signal axes IFN-γ/chemokines and IL-18 could be the immune-mediated mechanisms of HEV-induced renal disorder.

【 授权许可】

Unknown