Webinar – SFARI – Sarkis Mazmanian – Probiotics for Autism

Webinar: Sarkis Mazmanian explores probiotics for autism

http://sfari.org/sfari-community/webinar-series/2013/webinar-sarkis-mazmanian-explores-probiotics-for-autism/

“Mazmanian will discuss his lab’s investigation into the connection between gut bacteria, intestinal disease and autism — and how this work may lead to using probiotics to treat the disorder.”

Full Details at sfari link.

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Further Readings of Interest

Sarkis Mazmanian: Microbe Machinist

http://www.the-scientist.com/?articles.view/articleNo/34781/title/Sarkis-Mazmanian–Microbe-Machinist/

“Now in his own lab at the California Institute of Technology, Mazmanian has learned that PSA induces the development of immune cells called regulatory T cells (Tregs), which tell the immune response when to turn off.3 Dysfunction in Tregs is associated with numerous inflammatory, autoimmune, and allergic disorders in humans, and Mazmanian and his colleagues have shown that feeding PSA to a mouse with inflammatory bowel disease or multiple sclerosis can treat and even cure the ailments.”

The Sarkis Mazmanian lab – Caltech Biology

http://www.sarkis.caltech.edu/Welcome.html

Modeling an autism risk factor in mice leads to permanent immune dysregulation.

http://www.ncbi.nlm.nih.gov/pubmed/22802640

Biology Division, California Institute of Technology, Pasadena, CA

Abstract

Increasing evidence highlights a role for the immune system in the pathogenesis of autism spectrum disorder (ASD), as immune dysregulation is observed in the brain, periphery, and gastrointestinal tract of ASD individuals.

Furthermore, maternal infection (maternal immune activation, MIA) is a risk factor for ASD. Modeling this risk factor in mice yields offspring with the cardinal behavioral and neuropathological symptoms of human ASD.

In this study, we find that offspring of immune-activated mothers display altered immune profiles and function, characterized by a systemic deficit in CD4(+) TCRβ(+) Foxp3(+) CD25(+) T regulatory cells, increased IL-6 and IL-17 production by CD4(+) T cells, and elevated levels of peripheral Gr-1(+) cells.

In addition, hematopoietic stem cells from MIA offspring exhibit altered myeloid lineage potential and differentiation.

Interestingly, repopulating irradiated control mice with bone marrow derived from MIA offspring does not confer MIA-related immunological deficits, implicating the peripheral environmental context in long-term programming of immune dysfunction.

Furthermore, behaviorally abnormal MIA offspring that have been irradiated and transplanted with immunologically normal bone marrow from either MIA or control offspring no longer exhibit deficits in stereotyped/repetitive and anxiety-like behaviors, suggesting that immune abnormalities in MIA offspring can contribute to ASD-related behaviors.

These studies support a link between cellular immune dysregulation and ASD-related behavioral deficits in a mouse model of an autism risk factor.

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This entry was posted in Autism, co-morbid, Depression, diabetes, Environment, Epigenetics, Gut, Immune System, Inflammation, Mice, Muscular Dystrophy, Neurology, Physiology, Schizophrenia, Treatment. Bookmark the permalink.

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