Administration of Lactobacillus reuteri Combined with Clostridium butyricum Attenuates Cisplatin-Induced Renal Damage by Gut Microbiota Reconstitution, Increasing Butyric Acid Production, and Suppressing Renal Inflammation

Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus reuteri and Clostridium butyricum (LCs) had a protective effect on cisplatin-induced nephrotoxicity through reconstruction of gut microbiota...

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Published inNutrients Vol. 13; no. 8; p. 2792
Main Authors Hsiao, Yu-Ping, Chen, Hsiao-Ling, Tsai, Jen-Ning, Lin, Meei-Yn, Liao, Jiunn-Wang, Wei, Meng-Syuan, Ko, Jiunn-Liang, Ou, Chu-Chyn
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 15.08.2021
MDPI
Subjects
apoptosis
Bifidobacterium
blood
butyric acid
Cancer therapies
Chemotherapy
cisplatin
Clostridium butyricum
collagen
dysbiosis
endotoxins
Enterobacteriaceae
epithelium
Feces
fibronectins
fibrosis
Gut microbiota
Inflammation
intestinal microorganisms
intestines
Lactobacillus reuteri
microbiome
Microbiota
Mucositis
nephrotoxicity
oxidative stress
Probiotics
protective effect
Proteins
renoprotective effect
Ruminococcaceae
sulfates
Tumors
Minneapolis Minnesota
United Kingdom > UK
United States > US
Taiwan
Online AccessGet full text

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Abstract Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus reuteri and Clostridium butyricum (LCs) had a protective effect on cisplatin-induced nephrotoxicity through reconstruction of gut microbiota. Wistar rats were given different treatments: control, cisplatin (Cis), cisplatin + C. butyricum and L. reuteri (Cis+LCs), and C. butyricum and L. reuteri (LCs). We observed that cisplatin-treated rats supplemented with LCs exhibited significantly decreased renal inflammation (KIM-1, F4/80, and MPO), oxidative stress, fibrosis (collagen IV, fibronectin, and a-SMA), apoptosis, concentration of blood endotoxin and indoxyl sulfate, and increased fecal butyric acid production compared with those without supplementation. In addition, LCs improved the cisplatin-induced microbiome dysbiosis by maintaining a healthy gut microbiota structure and diversity; depleting Escherichia-Shigella and the Enterobacteriaceae family; and enriching probiotic Bifidobacterium, Ruminococcaceae, Ruminiclostridium_9, and Oscillibacter. Moreover, the LCs intervention alleviated the cisplatin-induced intestinal epithelial barrier impairment. This study indicated LCs probiotic serves as a mediator of the gut–kidney axis in cisplatin-induced nephrotoxicity to restore the intestinal microbiota composition, thereby suppressing uremic toxin production and enhancing butyrate production. Furthermore, the renoprotective effect of LCs is partially mediated by increasing the anti-inflammatory effects and maintaining the integrity of the intestinal barrier.
AbstractList Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus reuteri and Clostridium butyricum (LCs) had a protective effect on cisplatin-induced nephrotoxicity through reconstruction of gut microbiota. Wistar rats were given different treatments: control, cisplatin (Cis), cisplatin + C. butyricum and L. reuteri (Cis+LCs), and C. butyricum and L. reuteri (LCs). We observed that cisplatin-treated rats supplemented with LCs exhibited significantly decreased renal inflammation (KIM-1, F4/80, and MPO), oxidative stress, fibrosis (collagen IV, fibronectin, and a-SMA), apoptosis, concentration of blood endotoxin and indoxyl sulfate, and increased fecal butyric acid production compared with those without supplementation. In addition, LCs improved the cisplatin-induced microbiome dysbiosis by maintaining a healthy gut microbiota structure and diversity; depleting Escherichia-Shigella and the Enterobacteriaceae family; and enriching probiotic Bifidobacterium, Ruminococcaceae, Ruminiclostridium_9, and Oscillibacter. Moreover, the LCs intervention alleviated the cisplatin-induced intestinal epithelial barrier impairment. This study indicated LCs probiotic serves as a mediator of the gut-kidney axis in cisplatin-induced nephrotoxicity to restore the intestinal microbiota composition, thereby suppressing uremic toxin production and enhancing butyrate production. Furthermore, the renoprotective effect of LCs is partially mediated by increasing the anti-inflammatory effects and maintaining the integrity of the intestinal barrier.Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus reuteri and Clostridium butyricum (LCs) had a protective effect on cisplatin-induced nephrotoxicity through reconstruction of gut microbiota. Wistar rats were given different treatments: control, cisplatin (Cis), cisplatin + C. butyricum and L. reuteri (Cis+LCs), and C. butyricum and L. reuteri (LCs). We observed that cisplatin-treated rats supplemented with LCs exhibited significantly decreased renal inflammation (KIM-1, F4/80, and MPO), oxidative stress, fibrosis (collagen IV, fibronectin, and a-SMA), apoptosis, concentration of blood endotoxin and indoxyl sulfate, and increased fecal butyric acid production compared with those without supplementation. In addition, LCs improved the cisplatin-induced microbiome dysbiosis by maintaining a healthy gut microbiota structure and diversity; depleting Escherichia-Shigella and the Enterobacteriaceae family; and enriching probiotic Bifidobacterium, Ruminococcaceae, Ruminiclostridium_9, and Oscillibacter. Moreover, the LCs intervention alleviated the cisplatin-induced intestinal epithelial barrier impairment. This study indicated LCs probiotic serves as a mediator of the gut-kidney axis in cisplatin-induced nephrotoxicity to restore the intestinal microbiota composition, thereby suppressing uremic toxin production and enhancing butyrate production. Furthermore, the renoprotective effect of LCs is partially mediated by increasing the anti-inflammatory effects and maintaining the integrity of the intestinal barrier.
Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus reuteri and Clostridium butyricum (LCs) had a protective effect on cisplatin-induced nephrotoxicity through reconstruction of gut microbiota. Wistar rats were given different treatments: control, cisplatin (Cis), cisplatin + C. butyricum and L. reuteri (Cis+LCs), and C. butyricum and L. reuteri (LCs). We observed that cisplatin-treated rats supplemented with LCs exhibited significantly decreased renal inflammation (KIM-1, F4/80, and MPO), oxidative stress, fibrosis (collagen IV, fibronectin, and a-SMA), apoptosis, concentration of blood endotoxin and indoxyl sulfate, and increased fecal butyric acid production compared with those without supplementation. In addition, LCs improved the cisplatin-induced microbiome dysbiosis by maintaining a healthy gut microbiota structure and diversity; depleting Escherichia-Shigella and the Enterobacteriaceae family; and enriching probiotic Bifidobacterium , Ruminococcaceae , Ruminiclostridium_9 , and Oscillibacter . Moreover, the LCs intervention alleviated the cisplatin-induced intestinal epithelial barrier impairment. This study indicated LCs probiotic serves as a mediator of the gut–kidney axis in cisplatin-induced nephrotoxicity to restore the intestinal microbiota composition, thereby suppressing uremic toxin production and enhancing butyrate production. Furthermore, the renoprotective effect of LCs is partially mediated by increasing the anti-inflammatory effects and maintaining the integrity of the intestinal barrier.
Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus reuteri and Clostridium butyricum (LCs) had a protective effect on cisplatin-induced nephrotoxicity through reconstruction of gut microbiota. Wistar rats were given different treatments: control, cisplatin (Cis), cisplatin + C. butyricum and L. reuteri (Cis+LCs), and C. butyricum and L. reuteri (LCs). We observed that cisplatin-treated rats supplemented with LCs exhibited significantly decreased renal inflammation (KIM-1, F4/80, and MPO), oxidative stress, fibrosis (collagen IV, fibronectin, and a-SMA), apoptosis, concentration of blood endotoxin and indoxyl sulfate, and increased fecal butyric acid production compared with those without supplementation. In addition, LCs improved the cisplatin-induced microbiome dysbiosis by maintaining a healthy gut microbiota structure and diversity; depleting Escherichia-Shigella and the Enterobacteriaceae family; and enriching probiotic Bifidobacterium, Ruminococcaceae, Ruminiclostridium_9, and Oscillibacter. Moreover, the LCs intervention alleviated the cisplatin-induced intestinal epithelial barrier impairment. This study indicated LCs probiotic serves as a mediator of the gut–kidney axis in cisplatin-induced nephrotoxicity to restore the intestinal microbiota composition, thereby suppressing uremic toxin production and enhancing butyrate production. Furthermore, the renoprotective effect of LCs is partially mediated by increasing the anti-inflammatory effects and maintaining the integrity of the intestinal barrier.
Author Hsiao, Yu-Ping
Wei, Meng-Syuan
Tsai, Jen-Ning
Liao, Jiunn-Wang
Ko, Jiunn-Liang
Chen, Hsiao-Ling
Lin, Meei-Yn
Ou, Chu-Chyn
AuthorAffiliation 1 Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan; missyuping@gmail.com
6 Department of Food Science and Biotechnology, National Chung Hsing University, Taichung 40227, Taiwan; mylin@dragon.nchu.edu.tw (M.-Y.L.); priscillawie@gmail.com (M.-S.W.)
7 Graduate Institute of Veterinary Pathobiology, National Chung Hsing University, Taichung 40227, Taiwan; jwliao@dragon.nchu.edu.tw
10 Department of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan
2 Department of Dermatology, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
9 Department of Nutrition, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
3 Department of Food, Nutrition and Health Biotechnology, Asia University, Taichung 41354, Taiwan; hlchen908@asia.edu.tw
5 Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
8 Department of Medical Oncology and Chest Medicine, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
4 Department of
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PublicationPlace Basel
PublicationPlace_xml – name: Basel
PublicationTitle Nutrients
PublicationYear 2021
Publisher MDPI AG
MDPI
Publisher_xml – name: MDPI AG
– name: MDPI
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Snippet Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus...
Cisplatin-induced nephrotoxicity is associated with gut microbiota disturbance. The present study aimed to investigate whether supplementation of Lactobacillus...
SourceID pubmedcentral
proquest
crossref
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Aggregation Database
Enrichment Source
Index Database
StartPage 2792
SubjectTerms apoptosis
Bifidobacterium
blood
butyric acid
Cancer therapies
Chemotherapy
cisplatin
Clostridium butyricum
collagen
dysbiosis
endotoxins
Enterobacteriaceae
epithelium
Feces
fibronectins
fibrosis
Gut microbiota
Inflammation
intestinal microorganisms
intestines
Lactobacillus reuteri
microbiome
Microbiota
Mucositis
nephrotoxicity
oxidative stress
Probiotics
protective effect
Proteins
renoprotective effect
Ruminococcaceae
sulfates
Tumors
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Title Administration of Lactobacillus reuteri Combined with Clostridium butyricum Attenuates Cisplatin-Induced Renal Damage by Gut Microbiota Reconstitution, Increasing Butyric Acid Production, and Suppressing Renal Inflammation
URI https://www.proquest.com/docview/2565481890
https://www.proquest.com/docview/2566028166
https://www.proquest.com/docview/2636761782
https://pubmed.ncbi.nlm.nih.gov/PMC8402234
Volume 13
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