The interaction between intestinal microenvironment and stroke

Abstract

Background Stroke is not only a major cause of disability but also the third leading cause of death, following heart disease and cancer. It has been established that stroke causes permanent disability in 80% of survivors. However, current treatment options for this patient population are limited. Inflammation and immune response are major features that are well‐recognized to occur after a stroke. The gastrointestinal tract hosts complex microbial communities, the largest pool of immune cells, and forms a bidirectional regulation brain‐gut axis with the brain. Recent experimental and clinical studies have highlighted the importance of the relationship between the intestinal microenvironment and stroke. Over the years, the influence of the intestine on stroke has emerged as an important and dynamic research direction in biology and medicine. Aims In this review, we describe the structure and function of the intestinal microenvironment and highlight its cross‐talk relationship with stroke. In addition, we discuss potential strategies aiming to target the intestinal microenvironment during stroke treatment. Conclusion The structure and function of the intestinal environment can influence neurological function and cerebral ischemic outcome. Improving the intestinal microenvironment by targeting the gut microbiota may be a new direction in treating stroke.

Causal effects of gut microbiota on the prognosis of ischemic stroke: evidence from a bidirectional two-sample Mendelian randomization study

“…The intestinal barrier acts as the first barrier to prevent harmful substances from penetrating the intestinal mucosa and damaging other tissues of the body. The disruption of IEB after stroke contributes to the microbial translocation which will increase the risk of post-stroke infections (Zhao et al, 2023 ). Therefore, the protective effect of the genus Lachnospiraceae NK4A136 group on IEB may be helpful in IS prognosis.…”

Role of the gut microbiota in complications after ischemic stroke

“…Over 50% of patients with IS experience gastrointestinal complications, including swallowing difficulties, intestinal motility and absorption disorders, gastrointestinal bleeding, intestinal leakage, fecal incontinence, and intestinal septicemia (Durgan et al, 2019;Long et al, 2022). Extensive research in genomics, metabolomics, and proteomics has revealed that the gut microbiota is involved in several pathophysiological events following stroke, and patients with IS with gastrointestinal complications often have a poor prognosis, high mortality rate, and neurological function deterioration (Tuz et al, 2022;Zhao et al, 2023).…”

“…Following stroke, the gut microbiota is dysregulated, and the abundance of gram-negative Enterobacteriaceae increases (Huang and Xia, 2021). Multiple studies have shown a correlation between intestinal epithelial barrier dysfunction, intestinal leakage in patients with IS, and changes in the gut microbiota (Zhang et al, 2022), which can lead to intestinal villous epithelial damage, reduced mucus and expression of intestinal tight junction proteins, increased intestinal permeability, and intestinal sepsis (Zhao et al, 2023). The disruption of intestinal epithelial barrier function is associated with the LPS of gram-negative bacteria, metabolites of dominant bacterial populations such as SCFAs and TMAO, and intestinal inflammatory factors, including TNF-a, IL-1, IL-6, and nitric oxide synthase (Cheng et al, 2018;Chen et al, 2019c;Yu et al, 2021).…”

“…Reduction in SCFAs post IS has also been confirmed (Zou et al, 2022); SCFAs promote the development of the intestinal barrier and protect it against LPS damage by inhibiting NOD-like receptor thermal protein domainassociated protein 3 (NLRP3) inflammasomes (Figure 2). The intestinal immune system comprises multiple immune tissues and cells that cooperate under physiological conditions to resist pathogen invasion and maintain immune homeostasis (Pu et al, 2023;Zhao et al, 2023). Under normal physiological conditions, B cells differentiate into IgA-producing B cells in the presence of T cells to eliminate toxins and pathogens (Suzuki and Nakajima, 2014).…”