184
and impact functional outcome [146]. Dysbiosis of the gut microbiota has been reported in patients with several diseases including DM and stroke [147, 148]. In stroke patients, the three major beneficial microbes that were depleted include Bacteroides, Prevotella, and Faecalibacterium; while the major enriched microbes include the opportunistic pathogens Enterobacter, Megasphaera, and Desulfovibrio [147]. Increase in the abundance of Lactobacillus ruminis subgroup in the gut, may contribute to inflammation in stroke patients [149]. In mice subject to I/R injury, intestinal T cells traffic from the gut to the meninges of the brain; promote post-ischemic neuroinflam- mation by increasing pro-inflammatory cytokine IL-17; which can stimulate the pro- duction of several other cytokines and chemokines facilitating the infiltration of cytotoxic immune cells and neutrophils into the injured brain [145].
The gut microbial composition differs between DM and non DM patients [150].
It was found that, patients with low bacterial richness (low gene count) were more prone to obesity, insulin resistance, dyslipidemia, and inflammation compared to patients with a high gene count [150]. In a population of Chinese T2DM patients, moderate gut microbial dysbiosis was characterized by a decrease in beneficial bac- teria such as butyrate-producing bacteria that has protective role against several types of diseases; and an increase in diverse opportunistic pathogens [151]. In a group of Japanese T2DM patients, compared to control patients, an abundance of gut bacteria was found in the blood stream of T2DM patients, indicating bacterial translocation from the gut to the blood [152]. In T2DM patient, gut dysbiosis increases some microbial functions which leads to increased oxidative stress response, which may mediate the proinflammatory state in DM [151]. In DM mice subject to I/R injury, altering the gut microbiome via probiotic treatment restored the gut microbiome profile, significantly decreased behavioral deficits, decreased blood glucose levels, induced neuroprotection, and increased cell survival [143].
Extensive depletion of the gut microbiota significantly increases post stroke mortal- ity in mice, suggesting that conventional intestinal microbiota provides protection against ischemic damage, and that alterations to the gut microbiota can influence stroke outcome [153]. Future studies are required to understand the mechanisms of gut-brain axis and its impact on stroke in DM patients.
185 Acknowledgements None
Sources of funding This work was supported by National Institute of Neurological Disorders and Stroke R01 NS083078-01A1 (JC) and RO1 NS099030-01 (JC) and R01NS097747 (QJ/JC).
Disclosures None
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