MedicalResearch.com Interview with:
Dr. Josef Anrather
Josef Anrather, VMD
Finbar and Marianne Kenny Research Scholar
Associate Professor, Feil Family Brain and Mind Research Institute
Weill Cornell Medical College
New York, NY10065
MedicalResearch.com: What is the background for this study? What are the main findings?
Dr. Anrather: Worldwide, stroke is causing 5.6 million deaths annually. This ranks stroke as the second most common cause of death. Moreover, stroke is a leading cause of long-term disability. Stroke, even though primarily a vascular disease, has a strong inflammatory component both in rodent models and in clinics. While it is widely accepted that commensal bacteria shape the gastrointestinal immune system and have a strong impact on gastrointestinal immune diseases including Inflammatory Bowel Disease, Chron’s Disease and colitis, only recently it became evident that intestinal bacteria, at least in animal models, could alter disease course of a variety of autoimmune diseases including rheumatoid arthritis, diabetes, and multiple sclerosis. This was the point when our laboratory became interested in exploring the impact of intestinal bacteria on stroke. Although stroke is not an autoimmune disease and a role of the adaptive immune system during the acute phase of stroke is unlikely, we hypothesized that lymphoid cells more closely associated with the innate immune system, such as γδ T cells, might be also a target for intestinal bacteria.
Our study establishes a link between intestinal commensal bacteria and stroke outcome. Additionally, we show that immune cells in the gut matter and that the composition of intestinal immune cells has an impact on the immune response to stroke. One of the components identified by our study are γδ T cells which are regulated by the intestinal flora.
MedicalResearch.com: What should clinicians and patients take away from your report?
Dr. Anrather: The major message of our study is that stroke cannot be seen entirely as a isolated disease of the brain. There are components outside the brain that can influence the course and outcome of stroke. In our study we have identified the intestinal flora as a regulator of immune cells that participate in stroke. These immune cells are regulated in the gut through interaction with the commensal microbiota and can traffic to the meninges where they orchestrate the inflammatory response after stroke.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Dr. Anrather: Although the intestinal flora in humans seems relatively homogeneous among individuals at the phyla level, there is high inter-individual variation at lower taxonomic levels and only one third of bacterial genes are shared among individuals. This raises the question whether association with specific bacterial families or species could determine disease risk.
Future work will have to focus on establishing large population-level databases of enterotypes of the human gut microbiome, so we can use these epidemiological data to ask the question whether a certain microbial makeup is correlated with the frequency of cardiovascular events and – in the end – with stroke outcome. Once such microbial traits are identified there is the possibility of dietary or probiotic intervention to establish a flora with beneficial effect on the cardiovascular system.
MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.
Corinne Benakis, David Brea, Silvia Caballero, Giuseppe Faraco, Jamie Moore, Michelle Murphy, Giulia Sita, Gianfranco Racchumi, Lilan Ling, Eric G Pamer, Costantino Iadecola, Josef Anrather.
Commensal microbiota affects ischemic stroke outcome by regulating intestinal γδ T cells. Nature Medicine, 2016; DOI: 10.1038/nm.4068
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