Intestinal bacterial disorders can increase the risk of stroke and affect stroke outcomes

is a group of diseases with isoemia and hemorrhagic damage to the brain, with very high mortality and disability rates. Ished hemorrhagic stroke accounts for about 85% of all strokes, and the rest are hemorrhagic strokes. Isoemia stroke is a major global health problem, and the risk of stroke is likely to continue to increase as the population ages.years, the role of intestinal bacterios in the pathogenesis of disease and the potential of changing intestinal bacterios to treat diseases have attracted more and more attention. Intestinal bacteria play an important role in maintaining host health. A significant proportion of stroke patients suffer from gastrointestinal complications, including dysphagia, gastrointestinal bleeding, and constipation, which often adversely affect stroke outcomes. A growing body of research has found that the interaction between the gut bacteria and the brain play an important role in the occurrence of stroke and the outcome of stroke.intestinal bacteria increase the risk of stroke?triamide is one of the metabolites of gut microbes and one of the most thoroughly studied links between gut microbiomes and stroke risk. Early animal studies have shown that a diet rich in phosphatidylcholine, such as red meat, promotes atherosclerosis, in which the gut bacteriota play an important role in the metabolism of phosphatidylcholine. Intestinal microorganisms metabolize phosphatidylcholine in the diet, first forming triamcinoids, which are then converted into triamcinoxyamine by the leucin monooxygenase in the liver.A large clinical study followed more than 4,000 patients with selective coronary aneurysms for three years, assessing the relationship between levels of triamide oxide in an empty stomach plasma and major adverse cardiovascular events (death, myocardial infarction, or stroke). It was found that triamide oxidation produced by phosphatidylcholine in the diet depended on the metabolism of the intestinal bacterium, and the increase in triamide levels was associated with an increased risk of major adverse cardiovascular events. This link has been confirmed in other studies.case control study for patients with hypertension in China showed that higher levels of triamidamine oxidation were associated with an increased risk of stroke at first. Another study of patients with severe stenosis of the cervical artery who underwent a cervical stent implant reported that an increase in triamide levels after stent implantation was associated with an increased risk of new ischemia damage to the brain.the relationship between triamid oxide, atherosclerosis and stroke risk seems to have been well established, how does triamid oxide regulate the risk of atherosclerosis?1) One possible mechanism for increasing the risk of cardiovascular disease and atherosclerosis is an increase in inflammation of the inflammatory monocytes and blood vessels mediated by triamlamphetamine oxidation, as well as in ischemia stroke patients, where elevated levels of methamphetamine oxidation and a dose dependence on the risk of relapsed stroke. In addition, there was a significant correlation between triamlycamine levels and the percentage of monocytes that promote inflammation.2) Other mechanisms of methamphetamine oxide include its regulation of plateboard hyperreactiveness, cholesterol metabolism, and foam cell formation, which play a key role in the onset of atherosclerosis.3) In addition, plasma triamide levels have also been shown to be associated with other risk factors for isomorphic stroke, including atrial fibrillation and diabetes, which in themselves can lead to an increased risk of stroke.addition to triamide oxide, other studies have shown that patients have different gut bacteria depending on the risk of stroke. Specifically, in high-risk populations, the number of pathogenic bacteria increased significantly, while the number of bacteria producing butyric acid decreased significantly. As a result, changes in the composition of the gut bacteria may increase the risk of stroke.stroke cause an imbalance in the gut bacteria?acute isomorthic stroke can lead to intestinal bacteria disorders, which in turn affect the neural inflammatory process and the outcome of stroke., some animal-based studies have shown significant differences in intestinal bacterial composition between animal models after stroke and control groups. One study showed that after a stroke in mice caused by ischemia, there were substantial changes in the bacteribus in various parts of the gastrointestinal tract, even at bacterial gate levels, while changes in the composition of the intestinal mucosa caused by stroke were characterized by increased mucosal protein Almanella abundance and excessive reproduction of the Cytobacteria genus.another study using a stroke model of a mouse with arterial embolism in the brain found that three days after a severe stroke, there was a significant change in the composition of the gut bacteriocystus, mainly due to reduced species diversity and overgrowth of mycobacteria., clinical studies to evaluate changes in intestinal bacteria after stroke are still limited. A study that assessed fecal bacteria and fecal organic acids in stroke patients found a significant increase in the number of Lactobacillus ruminis in stroke patients compared to the control group; Although different studies have had less consistent results, there is no doubt that stroke can alter the composition of the intestinal bacteria in patients. , how does a stroke cause an imbalance in the gut bacteria? possible mechanism is that after an acute isomorthic stroke, the stress response after the stroke leads to reduced gastrointestinal movement, which can lead to overgrowth of bacteria. For example, reduced species diversity and overgrowth of mycobacterium bacteria observed in animal models are signs of intestinal bacteria disorders after stroke, which are associated with reduced intestinal movement. autonomic nervous system is also involved in regulating the effects of stroke on intestinal microbiosis imbalances. Stroke changes the composition of the blind enterobacteria group and vary depending on the severity of the injury, which is regulated by the release of epinephrine from the autonomic nervous system, as well as changes in the production of mucus proteins in the blind intestine and the number of cup cells. addition, stress response after stroke releases hormones and glucoticoids by releasing adrenal corticosteroids, increasing intestinal permeability and leading to an increase in the susceptible of gut bacteria. This is consistent with clinically reported increased gastrointestinal movement and gastrointestinal complications in patients with severe brain injury and isoemia stroke. other potential mechanisms associated with acute stroke and intestinal microbiota disorders include substances that directly affect the composition of the intestinal bacterium released by necrotic brain tissue, such as the release of adenosine triphosphate, high-migration family proteins B1 (HMGB1), S100 proteins, etc. that affect intestinal immunity and bacterial composition. does the intestinal bacteria affect stroke outcomes? changes in the gut bacteria can affect nerve inflammation after a stroke and affect the outcome of a stroke. Researchers first transplanted gut microbes from stroke mice and normal mice into sterile mice, and then induced them to have a stroke, and found that mice receiving gut microbes from stroke mice had significantly larger infarction areas than mice that received normal mice gut microbes. In addition, mice transplanted from stroke mice had higher expression of inflammatory T-cells. Within 2-3 days of a stroke, T-cells from the mice's intestines transfer to the brain, exacerbating nerve damage. In another animal study, the removal of gut microorganisms using broad-spectrum antibiotics (amoxicillin/claviric acid) before inducing stroke produced anti-inflammatory neurotail, reduced infarction area by 60% and retained sensory motor function. differences in the composition of intestinal bacteria in young mice and older mice, which were associated with increased inflammation and intestinal permeability. The intestinal bacteriota of young mice was altered by fecal transplantation, making it similar to that of older mice, and after inducing stroke through arterial embolism in the brain, the mortality rate was higher in mice, the motor function was more severely impaired, and the cytokine response was higher. Conversely, changing the intestinal bacteria of older mice to resemble those of young mice can improve survival and recovery after stroke. clinical studies on the correlation between intestinal bactericidal disorders and clinical outcomes after acute isomorthic stroke are relatively rare. A study in Japan reported that changes in the abundance of lactobacillus are positively related to serum IL-6 levels. In addition, ischemia stroke was associated with an increase in the concentration of fecal ephedrine (intestinal microbial metabolites), which was positively associated with levels of inflammatory markers such as highly sensitive C-reactive proteins and white blood cell counts. Therefore, intestinal bacterial imbalance in patients with isoemia stroke may affect the metabolism and inflammation of the host. , the researchers defined a parameter called SDI (Stroke Dysbiosis Index) based on the characteristics of intestinal gie disorders after a stroke to define the severity of intestinal microbiodis disorders, which can be used as independent predictive factors for severe stroke and early adverse consequences. Transplanting fecal bacteria from patients with higher SDI levels to sterile mice can lead to more severe brain damage and an increase in intestinal inflammatory T-cells. intestinal bacterios groups be used as a target for stroke treatment? the relationship between the intestinal bacteriobi and the occurrence and prognosis of stroke, providing a new potential target for stroke treatment. Early studies have shown that plasma levels of triamide oxide can be significantly suppressed after the use of broad-spectrum antibiotics, but rise after the antibiotic is deactivation, which limits its use, after all, long-term use of antibiotics may increase many other health risks. researchers have developed an inhibitor that can effectively inhibit the production of intestinal microbial dependence on triamide, which may reduce the risk of thrombosis and stroke. CutC/D is the key enzyme of gut bacteria using choline to produce methamphetamine, and in animal models, a single oral CutC/D inhibitor can significantly reduce plasma TMAO levels by up to 3 days, saving diet-induced plateboard reactive enhancement and thrombosis, and is not significantly toxic and does not increase the risk of bleeding. transplantation is the transplantation of fecal bacteria from healthy supplies into the intestines of diseased individuals, reconstructing the intestinal bacteriota of patients and achieving the goal of treating diseases. As a safe and effective method to treat relapsed Thyrobacteria infection, fecal transplantation has been widely used. In animal experiments, transplanting normal faeces can improve stroke outcomes. probiotics can improve the gut microbiotics, regulate the release of cytokines and affect neuro-inflammatory responses, and may therefore be another treatment strategy for acute stroke. Animal studies have shown that probiotic Clostridium difficile can reduce brain damage in mice caused by ischemia/refilling. Dung transplantation and probiotic interventions also lack clinical studies in stroke patients and deserve further study as an effective means of reducing the severity of stroke and promoting post-stroke recovery. diet is the main determining factor affecting the composition of the gut bacteria. In fact, dietary diversity is also associated with changes in triamcinoid levels, and large intakes of foods containing L-carnitine and phosphatidylcholine (such as red meat) can increase triamcinate oxide produced by gut microorganisms. A high-fat diet increases the concentration of methamphetamine oxide in the body, while a Mediterranean diet reduces the production of methamphetamine oxide. Therefore, diet control is an effective means of improving stroke, on the one hand, by reducing the production of methamphetamine oxide to reduce the risk of stroke, on the other hand, by improving the gut bacteria to improve stroke results and promote rehabilitation. Summary There is a close interaction between the intestinal bacteria and the brain, and since gastrointestinal complications are very common in stroke patients, the role of gut bacteria in the occurrence and prognosis of stroke is also of increasing concern. A growing body of research has found that changes in the intestinal bacteria may be a risk factor for acute isomorphic stroke, increasing the risk of stroke; Improving the gut bacteria may be important for reducing the risk of stroke, reducing the severity of stroke, and improving prognosis. :
Tan, B. Y. Q., et al. (2020). "Gut Microbiota and Stroke." Ann Indian Acad Neurol 23(2): 155-158.
Battaglini, D., et al. (2020). "Gut Microbiota in Acute Ischemic Stroke: From Pathophysiology to Therapeutic Implications." Front Neurol 11: 598.
。