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![Commensal microbiota affects ischemic stroke outcome by regulating intestinal [gamma][delta] T cells : Nature Medicine : Nature Publishing Group | Immunopathology & Immunotherapy | Scoop.it](https://img.scoop.it/TRrxkpys-j5OIm8p8x6Ztjl72eJkfbmt4t8yenImKBVvK0kTmF0xjctABnaLJIm9)
Alterations in the gut microbiota affect stroke outcomes via modulation of T cells, suggesting a gut-brain axis linking commensal microbes with the CNS. 
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In one of the largest studies of its kind ever conducted, an international team of scientists has thrown new light on the genetic basis of the inflammatory bowel diseases (IBD).
The complete Article in Nature: http://www.nature.com/nature/journal/v491/n7422/full/nature11582.html
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Dietary fibers are metabolized by the gut microbiota into short-chain fatty acids (SCFAs) and have protective effects in inflammatory bowel disease. Here Benjamin J Marsland and colleagues report that mice fed a high-fiber diet have an altered microbiota and are protected from allergic airway inflammation. The SCFA propionate regulated allergic inflammation, bone marrow hematopoiesis and dendritic cell function. Taken together, these findings suggest that metabolites produced by the gut microbiota can influence hematopoiesis and immune responses in the lung.
Alfredo Corell's insight:
Nature Medicine 20, 159–166 (2014) doi:10.1038/nm.3444
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Commensal gut bacteria impact the host immune system and can influence disease processes in several organs, including the brain. However, it remains unclear whether the microbiota has an impact on the outcome of acute brain injury. Here we show that antibiotic-induced alterations in the intestinal flora reduce ischemic brain injury in mice, an effect transmissible by fecal transplants. Intestinal dysbiosis alters immune homeostasis in the small intestine, leading to an increase in regulatory T cells and a reduction in interleukin (IL)-17–positive γδ T cells through altered dendritic cell activity. Dysbiosis suppresses trafficking of effector T cells from the gut to the leptomeninges after stroke. Additionally, IL-10 and IL-17 are required for the neuroprotection afforded by intestinal dysbiosis. The findings reveal a previously unrecognized gut-brain axis and an impact of the intestinal flora and meningeal IL-17+ γδ T cells on ischemic injury.