Selective Probiotic Treatment Positively Modulates the Microbiota–Gut–Brain Axis in the BTBR Mouse Model of Autism

Recent studies have shown promise for the use of probiotics in modulating behaviour through the microbiota–gut–brain axis. In the present study, we assessed the impact of two probiotic strains in mitigating autism-related symptomology in the BTBR T+ Itpr3tf/J mouse model of autism spectrum disorder...

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Published inBrain sciences Vol. 12; no. 6; p. 781
Main Authors Pochakom, Angela, Mu, Chunlong, Rho, Jong M., Tompkins, Thomas A., Mayengbam, Shyamchand, Shearer, Jane
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 14.06.2022
MDPI
Subjects
Autism
Behavior
Cytokines
Drinking water
Feces
Genomics
gut microbiota
Hyperactivity
Inflammation
Intestinal microflora
Laboratories
Metabolism
Metabolites
Microbiota
Mitochondria
Oxygen consumption
Phylogeny
Prefrontal cortex
Probiotics
rRNA 16S
Supplements
Canada
United States > US
Germany
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Abstract Recent studies have shown promise for the use of probiotics in modulating behaviour through the microbiota–gut–brain axis. In the present study, we assessed the impact of two probiotic strains in mitigating autism-related symptomology in the BTBR T+ Itpr3tf/J mouse model of autism spectrum disorder (ASD). Male juvenile BTBR mice were randomized into: (1) control, (2) Lr probiotic (1 × 109 CFU/mL Lacticaseibacillus rhamnosus HA-114), and (3) Ls probiotic groups (1 × 109 CFU/mL Ligilactobacillus salivarius HA-118) (n = 18–21/group), receiving treatments in drinking water for 4 weeks. Gut microbiota profiling by 16S rRNA showed Lr, but not Ls supplementation, to increase microbial richness and phylogenetic diversity, with a rise in potential anti-inflammatory and butyrate-producing taxa. Assessing serum and brain metabolites, Lr and Ls supplementation produced distinct metabolic profiles, with Lr treatment elevating concentrations of potentially beneficial neuroactive compounds, such as 5-aminovaleric acid and choline. As mitochondrial dysfunction is often observed in ASD, we assessed mitochondrial oxygen consumption rates in the prefrontal cortex and hippocampus. No differences were observed for either treatment. Both Lr and Ls treatment reduced behavioural deficits in social novelty preference. However, no changes in hyperactivity, repetitive behaviour, and sociability were observed. Results show Lr to impart positive changes along the microbiota–gut–brain axis, exhibiting beneficial effects on selected behaviour, gut microbial diversity, and metabolism in BTBR mice.
AbstractList Recent studies have shown promise for the use of probiotics in modulating behaviour through the microbiota–gut–brain axis. In the present study, we assessed the impact of two probiotic strains in mitigating autism-related symptomology in the BTBR T + Itpr3 tf /J mouse model of autism spectrum disorder (ASD). Male juvenile BTBR mice were randomized into: (1) control, (2) Lr probiotic (1 × 10 9 CFU/mL Lacticaseibacillus rhamnosus HA-114), and (3) Ls probiotic groups (1 × 10 9 CFU/mL Ligilactobacillus salivarius HA-118) (n = 18–21/group), receiving treatments in drinking water for 4 weeks. Gut microbiota profiling by 16S rRNA showed Lr , but not Ls supplementation, to increase microbial richness and phylogenetic diversity, with a rise in potential anti-inflammatory and butyrate-producing taxa. Assessing serum and brain metabolites, Lr and Ls supplementation produced distinct metabolic profiles, with Lr treatment elevating concentrations of potentially beneficial neuroactive compounds, such as 5-aminovaleric acid and choline. As mitochondrial dysfunction is often observed in ASD, we assessed mitochondrial oxygen consumption rates in the prefrontal cortex and hippocampus. No differences were observed for either treatment. Both Lr and Ls treatment reduced behavioural deficits in social novelty preference. However, no changes in hyperactivity, repetitive behaviour, and sociability were observed. Results show Lr to impart positive changes along the microbiota–gut–brain axis, exhibiting beneficial effects on selected behaviour, gut microbial diversity, and metabolism in BTBR mice.
Recent studies have shown promise for the use of probiotics in modulating behaviour through the microbiota–gut–brain axis. In the present study, we assessed the impact of two probiotic strains in mitigating autism-related symptomology in the BTBR T+ Itpr3tf/J mouse model of autism spectrum disorder (ASD). Male juvenile BTBR mice were randomized into: (1) control, (2) Lr probiotic (1 × 109 CFU/mL Lacticaseibacillus rhamnosus HA-114), and (3) Ls probiotic groups (1 × 109 CFU/mL Ligilactobacillus salivarius HA-118) (n = 18–21/group), receiving treatments in drinking water for 4 weeks. Gut microbiota profiling by 16S rRNA showed Lr, but not Ls supplementation, to increase microbial richness and phylogenetic diversity, with a rise in potential anti-inflammatory and butyrate-producing taxa. Assessing serum and brain metabolites, Lr and Ls supplementation produced distinct metabolic profiles, with Lr treatment elevating concentrations of potentially beneficial neuroactive compounds, such as 5-aminovaleric acid and choline. As mitochondrial dysfunction is often observed in ASD, we assessed mitochondrial oxygen consumption rates in the prefrontal cortex and hippocampus. No differences were observed for either treatment. Both Lr and Ls treatment reduced behavioural deficits in social novelty preference. However, no changes in hyperactivity, repetitive behaviour, and sociability were observed. Results show Lr to impart positive changes along the microbiota–gut–brain axis, exhibiting beneficial effects on selected behaviour, gut microbial diversity, and metabolism in BTBR mice.
Author Tompkins, Thomas A
Rho, Jong M
Mu, Chunlong
Shearer, Jane
Pochakom, Angela
Mayengbam, Shyamchand
AuthorAffiliation 1 Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada; chunlong.mu1@ucalgary.ca (C.M.); jshearer@ucalgary.ca (J.S.)
5 Faculty of Kinesiology, University of Calgary, Calgary, AB T2N 4N1, Canada
6 Alberta Children’s Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada
3 Lallemand Inc., Lallemand Bio-Ingredients, Montreal, QC H1W 2N8, Canada; ttompkins@lallemand.com
2 Departments of Neurosciences, Pediatrics and Pharmacology, University of California San Diego (UCSD), La Jolla, CA 92093, USA; jrho@health.ucsd.edu
4 Department of Biochemistry, Memorial University of Newfoundland, St. John’s, NL A1C 5S7, Canada; smayengbam@mun.ca
AuthorAffiliation_xml – name: 5 Faculty of Kinesiology, University of Calgary, Calgary, AB T2N 4N1, Canada
– name: 6 Alberta Children’s Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada
– name: 4 Department of Biochemistry, Memorial University of Newfoundland, St. John’s, NL A1C 5S7, Canada; smayengbam@mun.ca
– name: 2 Departments of Neurosciences, Pediatrics and Pharmacology, University of California San Diego (UCSD), La Jolla, CA 92093, USA; jrho@health.ucsd.edu
– name: 3 Lallemand Inc., Lallemand Bio-Ingredients, Montreal, QC H1W 2N8, Canada; ttompkins@lallemand.com
– name: 1 Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada; chunlong.mu1@ucalgary.ca (C.M.); jshearer@ucalgary.ca (J.S.)
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Snippet Recent studies have shown promise for the use of probiotics in modulating behaviour through the microbiota–gut–brain axis. In the present study, we assessed...
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StartPage 781
SubjectTerms Autism
Behavior
Cytokines
Drinking water
Feces
Genomics
gut microbiota
Hyperactivity
Inflammation
Intestinal microflora
Laboratories
Metabolism
Metabolites
Microbiota
Mitochondria
Oxygen consumption
Phylogeny
Prefrontal cortex
Probiotics
rRNA 16S
Supplements
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Title Selective Probiotic Treatment Positively Modulates the Microbiota–Gut–Brain Axis in the BTBR Mouse Model of Autism
URI https://www.proquest.com/docview/2679677392
https://search.proquest.com/docview/2681032990
https://pubmed.ncbi.nlm.nih.gov/PMC9220969
https://doaj.org/article/193a1a06abb24495a6c9e065bba771f0
Volume 12
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