Promising probiotics for the treatment of nephrotoxicity induced during immune-checkpoint therapy against cancers

Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Satoru Matsuda; Sayuri Yoshikawa; Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Satoru Matsuda

doi:10.3934/bioeng.2022019

AIMS Bioengineering

2022, Volume 9, Issue 3: 283-292. doi: 10.3934/bioeng.2022019

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Promising probiotics for the treatment of nephrotoxicity induced during immune-checkpoint therapy against cancers

Department of Food Science and Nutrition, Nara Women's University, Kita-Uoya Nishimachi, Nara 630-8506, Japan.

Received: 30 June 2022 Revised: 07 August 2022 Accepted: 22 August 2022 Published: 09 September 2022

The immune-related adverse events resulting from the therapy of immune checkpoint inhibitors could cause kidney injury. Inflammatory reprogramming of regulatory T helper (Treg) cells or type 17 T helper (Th17) cells might be involved in the pathogenesis of nephropathy. Accumulating evidence confirms a connection between the diversity of gut microbiota and kidney diseases, suggesting that successful modification of gut microbiota could attenuate kidney injury. In other words, certain gut microbiota could contribute to the protection of kidneys via the gut-kidney axis. It has been shown that the dysbiosis of gut microbiota might affect the gut-kidney axis, leading to nephrotoxicity. On the contrary, altered levels of D-amino acids, ROS, and SCFAs through the adjustment of gut microbiota might be relevant to the reduction of nephrotoxicity. Here, we have discussed and suggested the beneficial roles of gut microbiota in the prevention of the kidney injury induced during immune-checkpoint therapy.
- immune-related adverse events,
- immune checkpoint inhibitors,
- gut-kidney axis,
- gut-immune axis,
- short-chain fatty acids,
- D-amino acids,
- reactive oxygen species
Citation: Sayuri Yoshikawa, Kurumi Taniguchi, Haruka Sawamura, Yuka Ikeda, Ai Tsuji, Satoru Matsuda. Promising probiotics for the treatment of nephrotoxicity induced during immune-checkpoint therapy against cancers[J]. AIMS Bioengineering, 2022, 9(3): 283-292. doi: 10.3934/bioeng.2022019

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Abstract

The immune-related adverse events resulting from the therapy of immune checkpoint inhibitors could cause kidney injury. Inflammatory reprogramming of regulatory T helper (Treg) cells or type 17 T helper (Th17) cells might be involved in the pathogenesis of nephropathy. Accumulating evidence confirms a connection between the diversity of gut microbiota and kidney diseases, suggesting that successful modification of gut microbiota could attenuate kidney injury. In other words, certain gut microbiota could contribute to the protection of kidneys via the gut-kidney axis. It has been shown that the dysbiosis of gut microbiota might affect the gut-kidney axis, leading to nephrotoxicity. On the contrary, altered levels of D-amino acids, ROS, and SCFAs through the adjustment of gut microbiota might be relevant to the reduction of nephrotoxicity. Here, we have discussed and suggested the beneficial roles of gut microbiota in the prevention of the kidney injury induced during immune-checkpoint therapy.

Abbreviations

ATP

adenosine triphosphate

CTLA-4

cytotoxic T lymphocyte-associated protein 4

CKD

chronic kidney disease

DNA

deoxyribonucleic acid

FMT

fecal microbiota transplantation

GVHD

graft-versus-host disease

HDAC

histone deacetylase

PD-1

programmed cell death protein 1

PD-L1

programmed cell death ligand 1

ROS

reactive oxygen species

SOD

superoxide dismutase

Th1

type 1 T helper

Th17

type 17 T helper

Treg

regulatory T

Acknowledgments

This work was supported in part by a general grant from Nara Women's University in Japan.

Conflict of interest

The authors declare no conflict of interest.

Author contributions

Conceptualization, SY and SM; original draft preparation and editing, KT, HS, YI, AT and SM; visualization, SY and SM; supervision, SM. Each author (SY, KT, HS, YI, AT, SM) has participated sufficiently in the work of drafting the article and/or revising the article for the important rational content. All authors gave final approval of the version to be submitted.

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