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Lactobacillus acidophilus KBL409 protects against kidney injury via improving mitochondrial function with chronic kidney disease

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Abstract

Purpose

Recent advances have led to greater recognition of the role of mitochondrial dysfunction in the pathogenesis of chronic kidney disease (CKD). There has been evidence that CKD is also associated with dysbiosis. Here, we aimed to evaluate whether probiotic supplements can have protective effects against kidney injury via improving mitochondrial function.

Methods

An animal model of CKD was induced by feeding C57BL/6 mice a diet containing 0.2% adenine. KBL409, a strain of Lactobacillus acidophilus, was administered via oral gavage at a dose of 1 × 109 CFU daily. To clarify the underlying mechanisms by which probiotics exert protective effects on mitochondria in CKD, primary mouse tubular epithelial cells stimulated with TGF-β and p-cresyl sulfate were administered with butyrate.

Results

In CKD mice, PGC-1α and AMPK, key mitochondrial energy metabolism regulators, were down-regulated. In addition, mitochondrial dynamics shifted toward fission, the number of fragmented cristae increased, and mitochondrial mass decreased. These alterations were restored by KBL409 administration. KBL409 supplementation also improved defects in fatty acid oxidation and glycolysis and restored the suppressed enzyme levels involved in TCA cycle. Accordingly, there was a concomitant improvement in mitochondrial respiration and ATP production assessed by mitochondrial function assay. These favorable effects of KBL409 on mitochondria ultimately decreased kidney fibrosis in CKD mice. In vitro analyses with butyrate recapitulated the findings of animal study.

Conclusions

This study demonstrates that administration of the probiotic Lactobacillus acidophilus KBL409 protects against kidney injury via improving mitochondrial function.

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Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Funding

This research was supported by a faculty research grant of Yonsei University College of Medicine for 2021, Seoul, Korea (6-2021-0220).

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Author notes

  1. Jimin Park and Ki Heon Nam contributed equally to this work.

Authors and Affiliations

  1. Department of Internal Medicine, College of Medicine, Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical Science, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea

    Jimin Park, Bo Young Nam & Gyuri Kim

  2. Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA

    Jimin Park

  3. Division of Integrated Medicine, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea

    Ki Heon Nam

  4. Division of Nephrology, Soonchunhyang University Seoul Hospital, Seoul, Korea

    Hyoungnae Kim

  5. KoBiolabs, Inc., Seoul, Korea

    Ki Uk Lee, Seok Cheon Song, Tae-Wook Nam & GwangPyo Ko

  6. Department of Environmental Health Sciences, Graduate School of Public Health, Seoul National University, Seoul, Korea

    Woon-Ki Kim & GwangPyo Ko

  7. Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Korea

    Jung Tak Park, Tae-Hyun Yoo, Shin-Wook Kang & Seung Hyeok Han

Authors
  1. Jimin Park
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  2. Ki Heon Nam
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  3. Bo Young Nam
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Contributions

TN, GK, and SHH designed the study; JP, KHN, BYN, GK, SCS, WK, KUL, and TN carried out experiments; JP, KHN, BYN, SCS, WK, KUL, and TN made figures; JP, KHN, JTP, TY, SK, GK, and SHH analyzed the data; KHN, JP, and SHH drafted the manuscript; SCS, WK, KUL, TN, JTP, TY, SK, GK, and SHH revised the manuscript. All authors approved the final version of the manuscript.

Corresponding author

Correspondence to Seung Hyeok Han.

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Conflict of interest

GwangPyo Ko is a founder and board member of KoBioLabs, Inc., a company characterizing the role of host–microbiome interaction in chronic diseases. The other authors declare no competing interests.

Ethical approval

The animal study was reviewed and approved by Institutional Animal Care and Use Committee, Yonsei University (2018-0281).

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Park, J., Nam, K.H., Nam, B.Y. et al. Lactobacillus acidophilus KBL409 protects against kidney injury via improving mitochondrial function with chronic kidney disease. Eur J Nutr (2024). https://doi.org/10.1007/s00394-024-03408-9

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