The Gut Microbiome and Inflammation in Autism Spectrum Disorder
Location
White Top Mtn
Start Date
4-12-2019 9:00 AM
End Date
4-12-2019 2:30 PM
Poster Number
102
Faculty Sponsor’s Department
Health Sciences
Name of Project's Faculty Sponsor
Dr. Michelle Chandley
Type
Poster: Competitive
Project's Category
Neuroscience, Microbiology, Anatomy
Abstract or Artist's Statement
Autism spectrum disorder is a neurodevelopmental disorder marked by social deficits, obsessive behavior, and repetitive actions. It has been shown that there is a communication pathway between the brain and gut called the gut-brain axis. Communication is thought to occur between the bacterial collections known as the microbiota in the gut and the resident immune cells in the brain, microglia. It has been postulated that bacteria in the gut are capable of secreting signaling molecules that can induce increases in pro-inflammatory cytokines. Specific cytokines such as IL-1B and IL-17 will elicit microglia activation and will likely result in alterations in neurotransmission in the brain. The activation or prohibition of maturation of microglia can lead to severe developmental delays. Four animal models will be used for this experiment. C57 will be the control or wildtype model; valproic acid is an anti-seizure medication that will be given to pregnant mice to see effects on offspring. BTBR is the third model, which has been genetically bred to have a thinned corpus callosum. The last model is poly IC, which is a virus that will be injected into mothers. Brain tissue, blood, and fecal samples were collected from animals for each model 21 days after birth. An intense brain developmental procedure known as pruning is occurring at postnatal day 21 that would correlate with the pruning age of a young human child. Pruning is thought to be greatly influenced by immune activation. Immunohistochemistry for the microglial marker IBA-1 (N=4) and peripheral blood analysis for six cytokines (N=5) has been performed in male animals from the four groups. It is hypothesized that there will be an increase in pro-inflammatory cytokines in the blood and microglial activation in the brain. These studies are instrumental in the creation of future mechanistic strategies that may illuminate treatable signaling pathways for ASD.
The Gut Microbiome and Inflammation in Autism Spectrum Disorder
White Top Mtn
Autism spectrum disorder is a neurodevelopmental disorder marked by social deficits, obsessive behavior, and repetitive actions. It has been shown that there is a communication pathway between the brain and gut called the gut-brain axis. Communication is thought to occur between the bacterial collections known as the microbiota in the gut and the resident immune cells in the brain, microglia. It has been postulated that bacteria in the gut are capable of secreting signaling molecules that can induce increases in pro-inflammatory cytokines. Specific cytokines such as IL-1B and IL-17 will elicit microglia activation and will likely result in alterations in neurotransmission in the brain. The activation or prohibition of maturation of microglia can lead to severe developmental delays. Four animal models will be used for this experiment. C57 will be the control or wildtype model; valproic acid is an anti-seizure medication that will be given to pregnant mice to see effects on offspring. BTBR is the third model, which has been genetically bred to have a thinned corpus callosum. The last model is poly IC, which is a virus that will be injected into mothers. Brain tissue, blood, and fecal samples were collected from animals for each model 21 days after birth. An intense brain developmental procedure known as pruning is occurring at postnatal day 21 that would correlate with the pruning age of a young human child. Pruning is thought to be greatly influenced by immune activation. Immunohistochemistry for the microglial marker IBA-1 (N=4) and peripheral blood analysis for six cytokines (N=5) has been performed in male animals from the four groups. It is hypothesized that there will be an increase in pro-inflammatory cytokines in the blood and microglial activation in the brain. These studies are instrumental in the creation of future mechanistic strategies that may illuminate treatable signaling pathways for ASD.