Live Biotherapeutics Drug Discovery Service for Stroke

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Overview

Stroke is an acute cerebrovascular disease mainly manifested as occlusion of blood vessels in the brain. Stroke leads to intestinal motility disorders, increases the transport of microorganisms and their derived products, such as trimethylamine-N-oxide (TMAO) and lipopolysaccharide (LPS), into the bloodstream, and increases the permeability of the intestinal barrier. All these changes accelerate systemic inflammation and worsening of symptoms, ultimately leading to a poor prognosis. Neurological impairment caused by stroke affects the secretion of neurotransmitters and gastrointestinal hormones. The most common treatments for stroke are drug therapy and thrombolytic therapy. Neither approach carries a high risk of complications and thus does not improve stroke outcomes. Probiotics may represent another therapeutic strategy for acute stroke because of their ability to alter gut microbiota, modulate cytokine release, and influence neuroinflammatory responses.

The Pathophysiological Mechanisms Underlying Stroke-induced Gut Dysbiosis

Hemorrhagic stroke is caused by a rupture of a cerebral blood vessel, while ischemic stroke (IS) is caused by a clot or embolus blocking a cerebral artery. The pathophysiological mechanisms of stroke-induced intestinal dysbiosis include the destruction of the intestinal epithelial barrier, tight junction and adherens junction proteins, mucus secretion changes, intestinal motility disorders, local immune homeostasis changes, goblet cell loss, increased LPS level, and intestinal inflammation. Recent studies have shown that gut microbiota regulates the pathogenesis of IS through the microbiota-gut-brain axis (MGBA). Acute IS induces microbiota dysregulation (top-down signaling). Down-regulation of signaling and these resulting changes in the gut microbiome affect neuroinflammatory processes and stroke outcomes (bottom-up signaling).

Fig.1 There are several ways to control IS by restoring the dysbiotic gut. (Huang, 2022)Fig.1 There are several ways to control IS by restoring the dysbiotic gut.1

Alterations in the Gut Microbiota During IS

Stroke-induced alterations in mucosal microbiota composition are primarily characterized by increased abundances of Akkermansia muciniphila and Clostridial species. Studies have shown that brain IS leads to dysbiosis of the microbiota. There was a decrease in bacterial diversity in mouse feces, with a decrease in Firmicutes abundance and an excessive increase in Bacteroidetes. In addition, increased plasma LPS or inflammatory cytokines are closely associated with Bacteroidetes overgrowth, and LPS may play a key role in chronic systemic inflammation after stroke. Therefore, chronic systemic inflammation and post-stroke gut microbiota may be potential therapeutic targets for stroke.

Next-generation Probiotic Strains at Creative Biolabs

Creative Biolabs can offer a range of next-generation probiotics for live biotherapeutics research, including but not limited to the following, click on Probiotic Strains to check out more strains you might be interested in.

Our Services for the Following Type/Similar Stroke Research

Research Article Available Services
Effects of the oral ingestion of probiotics on brain damage in a transient model of focal cerebral ischemia in mice.2
Preventive effects of Bacillus licheniformis on heat stroke in rats by sustaining intestinal barrier function and modulating gut microbiota.3

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References

  1. Huang, Wenjing, et al. "Crosstalk between the gut and brain in ischemic stroke: mechanistic insights and therapeutic options." Mediators of Inflammation 2022 (2022).
  2. Akhoundzadeh, Kobra, et al. "Effects of the oral ingestion of probiotics on brain damage in a transient model of focal cerebral ischemia in mice." Iranian Journal of Medical Sciences 43.1 (2018): 32.
  3. Li, Lei, et al. "Preventive effects of bacillus licheniformis on heat stroke in rats by sustaining intestinal barrier function and modulating gut microbiota." Frontiers in Microbiology 12 (2021): 630841.

For Research Use Only. Not intended for use in food manufacturing or medical procedures (diagnostics or therapeutics). Do Not Use in Humans.

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