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Intestinal microbiota plays a role in the nutrient metabolism, modulation of the immune system, arthritis, obesity and
intestinal inflammation. In the literature, there have been huge differences in the same Atm deficient mice in different labs
reported. When our lab moved from Harvard to UCLA, we found a similar difference in genetic instability and longevity.
When we changed the intestinal microbiota back to conventional microbiota, we could reproduce the phenotype at Harvard.
We tested Atm deficient mice for genotoxicity, genetic instability, DNA damage, inflammation markers, cancer latency and
longevity, and high throughput sequencing of the intestinal microbiota. Isogenic mice from different housing facilities showed a
four fold difference in life expectancy, a 4.5 fold difference in genetic instability and DNA damage. The onset of lymphomas was
significantly 2 fold different. We sequenced the microbiota of both facilities and found Lactobacillus johnsonii 456 as dominant
bacterial strain in the health beneficial microbiota. Just this bacterium by itself reduced genotoxicity, reduced inflammation
and reduced levels of cytotoxic T cells in the liver and blood. We also found similar differences in Trp53 deficient and even
in wild type mice. The underlying mechanisms are probably due to inflammation promotion or suppression mediated by
the intestinal microbiota. The understanding of this effect may lead to a breakthrough in the understanding of the causes of
carcinogenesis, which might lead to prevention of AT, a currently incurable progressive disease and possibly other cancerprone
DNA repair deficient diseases or even wild type mice and people.
Biography
Robert H Schiestl has obtained his PhD from the University of Vienna. He was a Postdoctoral Fellow at Edmonton, Alberta, Rochester, NY, and Chapel Hill, NC, before being a Professor at Harvard, where he stayed for 10 years. Since 16 years, he is working as a Professor at UCLA with 200 publications, 11 patents and 5 startup companies.