Inhibition of Toll-like receptor 4 and Interleukin-1 receptor prevent SARS-CoV-2 mediated kidney injury.


Journal

Cell death discovery
ISSN: 2058-7716
Titre abrégé: Cell Death Discov
Pays: United States
ID NLM: 101665035

Informations de publication

Date de publication:
10 Aug 2023
Historique:
received: 08 11 2022
accepted: 27 07 2023
revised: 28 06 2023
medline: 11 8 2023
pubmed: 11 8 2023
entrez: 10 8 2023
Statut: epublish

Résumé

Acute kidney injury (AKI) is a common and severe complication of the coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly affects the glomerular and tubular epithelial cells to induce AKI; however, its pathophysiology remains unclear. Here, we explored the underlying mechanisms and therapeutic targets of renal involvement in COVID-19. We developed an in vitro human kidney cellular model, including immortalized tubular epithelial and endothelial cell lines, demonstrating that SARS-CoV-2 directly triggers cell death. To identify the molecular targets in the process of SARS-CoV-2-mediated cell injury, we performed transcriptional analysis using RNA sequencing. Tubular epithelial cells were more prone to dying by SARS-CoV-2 than endothelial cells; however, SARS-CoV-2 did not replicate in renal cells, distinct from VeroE6/transmembrane protease serine 2 cells. Transcriptomic analysis revealed increased inflammatory and immune-related gene expression levels in renal cells incubated with SARS-CoV-2. Toll-like receptor (TLR) 3 in renal cells recognized viral RNA and underwent cell death. Furthermore, analysis of upstream regulators identified several key transcriptional regulators. Among them, inhibition of the interleukin-1 receptor (IL-1R) and TLR4 pathways protects tubular epithelial and endothelial cells from injury via regulation of the signal transducer and activator of transcription protein-3/nuclear factor-kB pathway. Our results reveal that SARS-CoV-2 directly injures renal cells via the proinflammatory response without viral replication, and that IL-1R and TLR4 may be used as therapeutic targets for SARS-CoV-2 mediated kidney injury.

Identifiants

pubmed: 37563112
doi: 10.1038/s41420-023-01584-x
pii: 10.1038/s41420-023-01584-x
pmc: PMC10415265
doi:

Types de publication

Journal Article

Langues

eng

Pagination

293

Informations de copyright

© 2023. Cell Death Differentiation Association (ADMC).

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Auteurs

Daigo Nakazawa (D)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. daigo-na@med.hokudai.ac.jp.

Yohei Takeda (Y)

Research Center for Global Agromedicine, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan.
Department of Veterinary Medicine, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan.

Masatoshi Kanda (M)

Department of Rheumatology and Clinical Immunology, Sapporo Medical University, Sapporo, Japan.

Utano Tomaru (U)

Department of Pathology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Haruko Ogawa (H)

Department of Veterinary Medicine, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan.

Takashi Kudo (T)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Satoka Shiratori-Aso (S)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Kanako Watanabe-Kusunoki (K)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Yusho Ueda (Y)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Atsuko Miyoshi (A)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Fumihiko Hattanda (F)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Saori Nishio (S)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Ryo Uozumi (R)

Division of Laboratory and Transfusion Medicine, Hokkaido University Hospital, Sapporo, Japan.

Akihiro Ishizu (A)

Department of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.

Tatsuya Atsumi (T)

Department of Rheumatology, Endocrinology, and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Classifications MeSH