Ischemic stroke damages the intestinal mucosa and induces alteration of the intestinal lymphocytes and CCL19 mRNA in rats

Liu, Yaning; Luo, Shijian; Kou, Li; Tang, Chaogang; Huang, Ruxun; Pei, Zhong; Li, Zhendong

doi:10.1016/j.neulet.2017.08.061

Cited by 42 publications

(24 citation statements)

References 34 publications

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“…More recently, the exploration of stroke’s consequences on intestinal immunology and morphology have shown that the number of T lymphocytes in the Peyer’s patches increased, activating intestinal immunity, and that the recruitment involved one specific chemokine, CCL19. 172 This mediator is indeed expressed in the intestinal epithelium and involved in B and T lymphocyte recruitment. The link between stroke and intestinal immune system seems to occur via the intermediation of commensal microbiota, suggesting again that it is a key player in regulating and influencing disease processes in the brain.…”

Section: Brain-gut Axis In Strokementioning

confidence: 99%

Post-stroke remodeling processes in animal models and humans

Cirillo

Brihmat

Castel-Lacanal

et al. 2019

J Cereb Blood Flow Metab

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After cerebral ischemia, events like neural plasticity and tissue reorganization intervene in lesioned and non-lesioned areas of the brain. These processes are tightly related to functional improvement and successful rehabilitation in patients. Plastic remodeling in the brain is associated with limited spontaneous functional recovery in patients. Improvement depends on the initial deficit, size, nature and localization of the infarction, together with the sex and age of the patient, all of them affecting the favorable outcome of reorganization and repair of damaged areas. A better understanding of cerebral plasticity is pivotal to design effective therapeutic strategies. Experimental models and clinical studies have fueled the current understanding of the cellular and molecular processes responsible for plastic remodeling. In this review, we describe the known mechanisms, in patients and animal models, underlying cerebral reorganization and contributing to functional recovery after ischemic stroke. We also discuss the manipulations and therapies that can stimulate neural plasticity. We finally explore a new topic in the field of ischemic stroke pathophysiology, namely the brain-gut axis.

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Section: Brain-gut Axis In Strokementioning

confidence: 99%

Post-stroke remodeling processes in animal models and humans

Cirillo

Brihmat

Castel-Lacanal

et al. 2019

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…As many as 50% of stroke survivors also experience GI complications, which results in a higher risk of mortality and worsened neurologic outcomes in these patients [3,4]. While several studies have revealed damage to the intestinal mucosa soon after experimental stroke [79,80], fewer studies have shown long-term effects. We observed that prolonged intestinal inflammatory pathology accompanies the changes that we see in bacterial abundance.…”

Section: Cells and Significant Increases In Cd4+ T Cells And Cd8+ T mentioning

confidence: 99%

Experimental Stroke Induces Chronic Gut Dysbiosis and Neuroinflammation in Male Mice

Brichacek¹,

Nwafor²,

Benkovic³

et al. 2020

Preprint

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Recent literature implicates gut epithelia mucosa and intestinal microbiota as important players in post-stroke morbidity and mortality. As most studies have focused on the acute effects of stroke on gut dysbiosis, our study objective was to measure chronic, longitudinal changes in the gut microbiota and intestinal pathology following ischemic stroke. We hypothesized that mice with experimental ischemic stroke would exhibit chronic gut dysbiosis and intestinal pathology up to 36 days post-stroke compared to sham controls. Male C57BL/6J mice were subjected to 60 minutes of transient middle cerebral artery occlusion (tMCAO) or sham surgery. To determine the long-term effects of tMCAO on gut dysbiosis, fecal boli were collected pre- and post-tMCAO on days 0, 3, 14, and 28. Bioinformatics analysis demonstrate significant differences in abundance among Firmicutes and Bacteroidetes taxa at the phylum, family, and species levels in tMCAO compared to sham mice that persisted up to one month post-stroke. The most persistent changes in post-stroke microbial abundance were a decrease in bacteria family S24-7 and significant increases in Ruminococcaceae. Overall, these changes resulted in a persistently increased Firmicutes:Bacteroidetes ratio in stroke animals. Intestinal histopathology showed evidence of chronic intestinal inflammation that included marked increases in immune cell infiltration with mild-moderate epithelial hyperplasia and villous blunting. Increased astrocyte and microglial activity were also detected one-month post-stroke. These results demonstrate that acute, post-stroke disruption of the gut-brain-microbiota axis progresses to chronic gut dysbiosis, intestinal inflammation, and chronic neuroinflammation.Clinical PerspectivesThe microbiota-gut-brain axis, recently implicated in several neurological disorders, remains largely unexplored at chronic time points post-tMCAO.Our results demonstrate chronic gut dysbiosis, prolonged behavioral deficits, and persistent cerebral and intestinal inflammation post-tMCAO in male C57BL/6J mice.These results suggest that manipulation of microbiota may help reduce poor outcomes after stroke and lead to improved post-stroke functional recovery.

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“…Alternation in intestinal microenvironment is an important pathophysiological consequence of acute ischemic stroke with direct evidence from both experimental models and clinical data. Those changes in MCAO mice include (1) increased gut permeability, (2) impaired gut motility, (3) gut dysbiosis (4) necrosis and shedding of the intestinal epithelium, (5) enteric neuronal loss, and (6) changes in T and B cells in Peyer’s patches (PPs) [79–83]. In patients with acute ischemic stroke, lipopolysaccharide-binding protein (LBP) was associated with both systemic inflammation and a predictive risk of post-stroke infections, which indicates a dysfunction in the intestinal barrier [84].…”

Section: Targeting Gbmax In Ischemic Strokementioning

confidence: 99%

Bidirectional gut-brain-microbiota axis as a potential link between inflammatory bowel disease and ischemic stroke

Zhao¹,

Xiong²,

Stary³

et al. 2018

J Neuroinflammation

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Emerging evidence suggests that gut-brain-microbiota axis (GBMAx) may play a pivotal role linking gastrointestinal and neuronal disease. In this review, we summarize the latest advances in studies of GBMAx in inflammatory bowel disease (IBD) and ischemic stroke. A more thorough understanding of the GBMAx could advance our knowledge about the pathophysiology of IBD and ischemic stroke and help to identify novel therapeutic targets via modulation of the GBMAx.

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Ischemic stroke damages the intestinal mucosa and induces alteration of the intestinal lymphocytes and CCL19 mRNA in rats

Cited by 42 publications

References 34 publications

Post-stroke remodeling processes in animal models and humans

Post-stroke remodeling processes in animal models and humans

Experimental Stroke Induces Chronic Gut Dysbiosis and Neuroinflammation in Male Mice

Bidirectional gut-brain-microbiota axis as a potential link between inflammatory bowel disease and ischemic stroke

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