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 in | Brain sciences Vol. 12; no. 6; p. 781 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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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. |
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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.) |
Author_xml | – sequence: 1 givenname: Angela orcidid: 0000-0002-2480-069X surname: Pochakom fullname: Pochakom, Angela – sequence: 2 givenname: Chunlong orcidid: 0000-0001-9405-5907 surname: Mu fullname: Mu, Chunlong – sequence: 3 givenname: Jong M. orcidid: 0000-0001-9886-9924 surname: Rho fullname: Rho, Jong M. – sequence: 4 givenname: Thomas A. orcidid: 0000-0002-2990-2265 surname: Tompkins fullname: Tompkins, Thomas A. – sequence: 5 givenname: Shyamchand surname: Mayengbam fullname: Mayengbam, Shyamchand – sequence: 6 givenname: Jane orcidid: 0000-0002-1224-979X surname: Shearer fullname: Shearer, Jane |
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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 |
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