GNPS_CalTech_murine_model_autism_study_1st_set
Ontology highlight
ABSTRACT:
INSTRUMENT(S): maXis
ORGANISM(S): Mus Musculus (ncbitaxon:10090)
SUBMITTER: 
Pieter Dorrestein
PROVIDER: MSV000082000 | GNPS | Tue Jan 30 21:28:00 GMT 2018
REPOSITORIES: GNPS
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Project description:<p class='ql-align-justify'><strong>Background</strong>: Autism spectrum disorder (ASD) is biologically heterogeneous and has limited mechanism-informed interventions targeting core behavioral symptoms. Emerging evidence suggests that gut microbial metabolism shapes neurobehavioral outcomes, yet the specific metabolic pathways linking gut ecology to brain function remain incompletely understood. One candidate pathway is polyamine metabolism, which links microbial amino acid metabolism to host regulation and represents a plausible but underexplored contributor to ASD-related phenotypes. Notably, the psychobiotic <em>Lactiplantibacillus plantarum</em> PS128 has been reported to improve social behaviors in individuals with ASD, although the molecular basis for these effects is unclear. In this study, we used Fragile X mental retardation 1 knockout (<em>Fmr1</em> KO) mice, a well-established ASD model, to investigate microbiota-dependent metabolic mechanisms underlying autism-like behaviors.</p><p class='ql-align-justify'><strong>Results</strong>: We found that autism-like behaviors in <em>Fmr1</em> KO mice were associated with gut dysbiosis, impaired intestinal barrier integrity, disruption of the arginine-ornithine-polyamine pathway, and elevated putrescine in the prefrontal cortex (PFC). Supplementation with PS128 remodeled the gut microbiota, reduced inflammation- and disease-associated taxa, improved intestinal structure and permeability, and restored polyamine homeostasis. Targeted metabolomics revealed an increased PFC-to-serum putrescine ratio in KO mice, which was normalized following PS128 intervention. This correction was accompanied by reduced expression of polyamine transporters in the PFC, including ATP13A family members. Causal experiments supported a functional role for putrescine, as peripheral elevation of putrescine induced autism-like behaviors in wild-type mice, whereas pharmacological inhibition of putrescine synthesis ameliorated behavioral deficits in <em>Fmr1</em> KO mice.</p><p class='ql-align-justify'><strong>Conclusions</strong>: These findings identify putrescine metabolic dysregulation as a key contributor to autism-like phenotypes and support the existence of an ASD subtype defined by disruption of the arginine-ornithine-polyamine axis. Integrated multi-omics and causal perturbation analyses support a model in which microbiota-targeted intervention rebalances systemic polyamine regulation along the gut-brain axis, thereby improving ASD-relevant behaviors. Our work provides mechanistic evidence linking microbial metabolism to neurochemical homeostasis and highlights the translational potential of metabolic stratification in ASD.</p><p class='ql-align-justify'><br></p><p><strong>UHPLC-MS/MS</strong> analysis of murine <strong>blood serum</strong> are reported in this study</p><p><strong>UHPLC-MS/MS</strong> analysis of murine<strong> brain tissues</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS13881' rel='noopener noreferrer' target='_blank'><strong>MTBLS13881</strong></a></p><p class='ql-align-justify'><strong>GC-MS </strong>analysis of murine <strong>brain tissues</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS13859' rel='noopener noreferrer' target='_blank'><strong>MTBLS13859</strong></a></p>
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Project description:<p><strong>Background </strong>Autism spectrum disorder (ASD) is biologically heterogeneous and has limited mechanism-informed interventions targeting core behavioral symptoms. Emerging evidence suggests that gut microbial metabolism shapes neurobehavioral outcomes, yet the specific metabolic pathways linking gut ecology to brain function remain incompletely understood. One candidate pathway is polyamine metabolism, which links microbial amino acid metabolism to host regulation and represents a plausible but underexplored contributor to ASD-related phenotypes. Notably, the psychobiotic Lactiplantibacillus plantarum PS128 has been reported to improve social behaviors in individuals with ASD, although the molecular basis for these effects is unclear. In this study, we used Fragile X mental retardation 1 knockout (Fmr1 KO) mice, a well-established ASD model, to investigate microbiota-dependent metabolic mechanisms underlying autism-like behaviors. </p><p><strong>Results </strong>We found that autism-like behaviors in Fmr1 KO mice were associated with gut dysbiosis, impaired intestinal barrier integrity, disruption of the arginine–ornithine–polyamine pathway, and elevated putrescine in the prefrontal cortex (PFC). Supplementation with PS128 remodeled the gut microbiota, reduced inflammation- and disease-associated taxa, improved intestinal structure and permeability, and restored polyamine homeostasis. Targeted metabolomics revealed an increased PFC-to-serum putrescine ratio in KO mice, which was normalized following PS128 intervention. This correction was accompanied by reduced expression of polyamine transporters in the PFC, including ATP13A family members. Causal experiments supported a functional role for putrescine, as peripheral elevation of putrescine induced autism-like behaviors in wild-type mice, whereas pharmacological inhibition of putrescine synthesis ameliorated behavioral deficits in Fmr1 KO mice.</p><p><strong>Conclusions </strong>These findings identify putrescine metabolic dysregulation as a key contributor to autism-like phenotypes and support the existence of an ASD subtype defined by disruption of the arginine–ornithine–polyamine axis. Integrated multi-omics and causal perturbation analyses support a model in which microbiota-targeted intervention rebalances systemic polyamine regulation along the gut–brain axis, thereby improving ASD-relevant behaviors. Our work provides mechanistic evidence linking microbial metabolism to neurochemical homeostasis and highlights the translational potential of metabolic stratification in ASD. </p><p><br></p><p><strong>GC-MS</strong> analysis of murine <strong>brain tissues</strong> are reported in in this study</p><p><strong>UHPLC-MS/MS</strong> analysis of murine <strong>brain tissues</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS13881' rel='noopener noreferrer' target='_blank'><strong>MTBLS13881</strong></a></p><p><strong>UHPLC-MS/MS </strong>analysis of murine <strong>blood serum</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS13862' rel='noopener noreferrer' target='_blank'><strong>MTBLS13862</strong></a></p>
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