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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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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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Largest Microbiome Study on Newly Diagnosed Patients Gives Insight Into Crohn's Disease and Shows Antibiotic Treatment May Worsen Disease
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Summary
Inflammatory bowel diseases (IBDs), including Crohn’s disease (CD), are genetically linked to host pathways that implicate an underlying role for aberrant immune responses to intestinal microbiota. However, patterns of gut microbiome dysbiosis in IBD patients are inconsistent among published studies. Using samples from multiple gastrointestinal locations collected prior to treatment in new-onset cases, we studied the microbiome in the largest pediatric CD cohort to date. An axis defined by an increased abundance in bacteria which include Enterobacteriaceae, Pasteurellacaea, Veillonellaceae, and Fusobacteriaceae, and decreased abundance in Erysipelotrichales, Bacteroidales, and Clostridiales, correlates strongly with disease status. Microbiome comparison between CD patients with and without antibiotic exposure indicates that antibiotic use amplifies the microbial dysbiosis associated with CD. Comparing the microbial signatures between the ileum, the rectum, and fecal samples indicates that at this early stage of disease, assessing the rectal mucosal-associated microbiome offers unique potential for convenient and early diagnosis of CD. Divulgative news: http://www.sys-con.com/node/3009818
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This study examines differences in microbial colonization and community stability in PID skin and informs our understanding of host–microbiome interactions, suggesting a bidirectional dialogue between skin commensals and the host organism.
Alfredo Corell's insight:
The altered landscape of the human skin microbiome in patients with primary immunodeficienciesJulia Oh1, Alexandra F. Freeman2, NISC Comparative Sequencing Program3, Morgan Park3, Robert Sokolic1, Fabio Candotti1,Steven M. Holland2, Julia A. Segre1,5,6 and Heidi H. Kong4,5,6Article published online before print. Article, supplemental material, and publication date are athttp://www.genome.org/cgi/doi/10.1101/gr.159467.113.
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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.