Project Title

Short-Chain Fatty Acid Profiles for Mouse Models of Autism Spectrum Disorder

Authors' Affiliations

Kyla Scott, Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN. Brooke Beasley, Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN. John Sterrett, Department of Allied Health Sciences, College of Clinical and Rehabilitative Health Sciences, East Tennessee State University, Johnson City, TN. Drew Gill, Biomedical Sciences, Quillen College of Medicine, Johnson City, TN. Dr. W. Andrew Clark, Department of Allied Health Sciences, College of Clinical and Rehabilitative Health Sciences, East Tennessee State University, Johnson City, TN. Michelle Chandley, Department of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN.

Location

Ballroom

Start Date

4-12-2019 9:00 AM

End Date

4-12-2019 2:30 PM

Poster Number

27

Faculty Sponsor’s Department

Health Sciences

Name of Project's Faculty Sponsor

Dr. Michelle Chandley

Type

Poster: Competitive

Classification of First Author

Undergraduate Student

Project's Category

Microbiology, Developmental Disabilities

Abstract Text

The microbiota-gut-brain axis is a multidirectional communication chain between the central and enteric nervous systems that relates brain function to peripheral intestinal functions. Gut microbiome composition is influential within the axis because different bacteria produce different shortchain fatty acid markers. Short-chain fatty acids can cross the blood-brain barrier to induce neuroinflammation and likely affect neural development. Autism spectrum disorder (ASD) is a neurodevelopmental disorder that has no defined etiology, cure, or therapeutic treatment. Neuroinflammation, microbiome alterations, and social deficits have been demonstrated in ASD. It is tempting to speculate that neuroinflammation caused by peripheral inflammation or microbiome products can induce abnormal brain development that results in social behavior deficits. However, to contribute to the previous statement a suitable animal model must be used. The current study uses three popular animal models that demonstrate social behavior deficits to determine if short-chain fatty acid profiles are different between the two models as well as a wild-type control strain. Fecal samples were collected from the following mouse strains between 90 and 120 days of development: C57BL/6J control mice, BTBR genetic knockout mice, C57BL/6J injected with valproic acid, and C57BL/6J injected with polycytidylic acid. The last two models were pregnant dams injected during day 11 of gestation. Short-chain fatty acid profiles were obtained from fecal samples to determine differences between the models. Percentages were obtained for the following short-chain fatty acids: acetic, propionic, isobutyric, butyric, isovaleric, and valeric acids. With this research, developmental cues that attribute to autism spectrum disorders may be better understood and, in the future, new preventative treatments may be advanced.

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Apr 12th, 9:00 AM Apr 12th, 2:30 PM

Short-Chain Fatty Acid Profiles for Mouse Models of Autism Spectrum Disorder

Ballroom

The microbiota-gut-brain axis is a multidirectional communication chain between the central and enteric nervous systems that relates brain function to peripheral intestinal functions. Gut microbiome composition is influential within the axis because different bacteria produce different shortchain fatty acid markers. Short-chain fatty acids can cross the blood-brain barrier to induce neuroinflammation and likely affect neural development. Autism spectrum disorder (ASD) is a neurodevelopmental disorder that has no defined etiology, cure, or therapeutic treatment. Neuroinflammation, microbiome alterations, and social deficits have been demonstrated in ASD. It is tempting to speculate that neuroinflammation caused by peripheral inflammation or microbiome products can induce abnormal brain development that results in social behavior deficits. However, to contribute to the previous statement a suitable animal model must be used. The current study uses three popular animal models that demonstrate social behavior deficits to determine if short-chain fatty acid profiles are different between the two models as well as a wild-type control strain. Fecal samples were collected from the following mouse strains between 90 and 120 days of development: C57BL/6J control mice, BTBR genetic knockout mice, C57BL/6J injected with valproic acid, and C57BL/6J injected with polycytidylic acid. The last two models were pregnant dams injected during day 11 of gestation. Short-chain fatty acid profiles were obtained from fecal samples to determine differences between the models. Percentages were obtained for the following short-chain fatty acids: acetic, propionic, isobutyric, butyric, isovaleric, and valeric acids. With this research, developmental cues that attribute to autism spectrum disorders may be better understood and, in the future, new preventative treatments may be advanced.