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Dr. Denis Gris has started his scientific career with the Master's and Ph.D. in Neuroscience at Dr. Lynn Weaver's laboratory at the University of Western Ontario. He studied the role of inflammation in spinal cord injury. He discovered that the influx of neutrophils is detrimental for recovering after spinal cord injury. Using anti CD11d antibody as a treatment, he demonstrated that animals recovered faster and better after the treatment. Also, he showed that sever spinal cord injury results in massive inflammatory reactions throughout the body leading to syndrome similar to multiple organ dysfunction syndrome. Dr. Denis Gris continued his education in Dr. Jenny P-Y Ting's laboratory as a post doctoral fellow at the University of North Carolina at Chapel Hill. There he studied in detail mechanism of activation of innate and adoptive immune responses. In collaboration with Dr. Wen, Dr. Eitas, Dr. Allen, and other members of the laboratory, Dr. Gris studied inflammation during obesity which leads to insulin resistance; innate and adoptive responses during multiple sclerosis. In summary, his role in this laboratory was to define the role of novel family of immuno regulatory proteins (NLRs) in different human diseases. Currently, Dr. Denis Gris is a member of Immunology Program at the University of Sherbrooke and he is studying neuro-immune interactions during healthy state and disease.
Cyanotoxins have been shown to be highly toxic for mammalian cells, including brain cells. However, little is known about their effect on inflammatory pathways. Our study investigated whether mammalian brain and immune cells can be a target of certain cyanotoxins, at doses approximating those in the guideline levels for drinking water. We examined the effects on cellular viability, apoptosis, and inflammation signaling of several toxins on murine macrophage-like RAW264.7, microglial BV-2, and neuroblastoma N2a cell lines. We have tested cylindrospermopsin (CYN), microcystin-LR (MC-LR), and anatoxin-a (ATXa), individually as well as in mixture. Searching into protective mechanism against cyanotoxins, we found that Nlrx1, a protein localized to mitochondria, ameliorates toxin effects. Decreased expression of Nlrx1 correlated with increased vulnerability of all cell types to toxin exposure. Our results demonstrate that CYN, MC-LR, and ATX-a, at low doses individually and in mixture, have potent effect inducing apoptosis and inflammation. Further research of the neuroinflammatory effects of these compounds in-vivo is needed to improve safety limit levels for cyanotoxins in drinking water and food.