Abstract
Background and Purpose: The gut communicates with the brain bidirectionally via neural, humoral and immune pathways. All these pathways are affected by acute brain lesions, such as stroke. Brain-gut communication may therefore impact on the overall outcome after CNS-injury. Until now, contradictory reports on intestinal function and translocation of gut bacteria after experimental stroke have been published. Accordingly, we aimed to specifically investigate the effects of transient focal cerebral ischemia on intestinal permeability, gut associated lymphoid tissue and bacterial translocation in an exploratory study using a well-characterized murine stroke model.Methods: After 60 min of middle cerebral artery occlusion (MCAO) we assessed intestinal morphology (time points after surgery day 0, 3, 5, 14, 21) and tight junction protein expression (occludin and claudin-1 at day 1 and 3) in 12-week-old male C57Bl/6J mice. Lactulose/mannitol/sucralose test was performed to assess intestinal permeability 24–72 h after surgery. To investigate the influence of cerebral ischemia on the local immune system of the gut, main immune cell populations in Peyer's patches (PP) were quantified by flow cytometry. Finally, we evaluated bacterial translocation to extraintestinal organs 24 and 72 h after MCAO by microbiological culture and fluorescence in situ hybridization targeting bacterial 16S rRNA.Results: Transient MCAO decreased claudin-1 expression in the ileum but not in the colon. Intestinal morphology (assessed by light microscopy) and permeability did not change measurably after MCAO. After MCAO, animals had significantly fewer B cells in PP compared to naïve mice.Conclusions: In a murine model of stroke, which leads to large brain infarctions in the middle cerebral artery territory, we did not find evidence for overt alterations neither in gut morphology, barrier proteins and permeability nor presence of intestinal bacterial translocation.
Highlights
Every year around 17 million people worldwide suffer their first stroke
To evaluate the influence of cerebral ischemia on intestinal morphology, we examined histological changes in the entire intestine with hematoxylin & eosin staining
Within the first 3 weeks after cerebral ischemia, we found no apparent evidence of disarrangement, erosion, ulceration and inflammation in intestinal submucosa and mucosa including epithelial cells and lamina propria. (Figures 1, Supplemental Figure 2)
Summary
Every year around 17 million people worldwide suffer their first stroke. Stroke patients are highly susceptible to medical complications, which influence outcome and increase the length of hospital stay, economic costs of treatment and burden of care given [1]. Recent evidence suggests that the population of commensal gut bacteria is profoundly disturbed after stroke. This may affect outcome after brain injury, mainly by interaction with the host immune system [8,9,10]. The gut communicates with the brain bidirectionally via neural, humoral and immune pathways All these pathways are affected by acute brain lesions, such as stroke. We aimed to investigate the effects of transient focal cerebral ischemia on intestinal permeability, gut associated lymphoid tissue and bacterial translocation in an exploratory study using a well-characterized murine stroke model
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