Abstract
Acute central nervous system (CNS) injuries, including stroke, traumatic brain injury (TBI), and spinal cord injury (SCI), are the common causes of death or lifelong disabilities. Research into the role of the gut microbiota in modulating CNS function has been rapidly increasing in the past few decades, particularly in animal models. Growing preclinical and clinical evidence suggests that gut microbiota is involved in the modulation of multiple cellular and molecular mechanisms fundamental to the progression of acute CNS injury-induced pathophysiological processes. The altered composition of gut microbiota after acute CNS injury damages the equilibrium of the bidirectional gut-brain axis, aggravating secondary brain injury, cognitive impairments, and motor dysfunctions, which leads to poor prognosis by triggering pro-inflammatory responses in both peripheral circulation and CNS. This review summarizes the studies concerning gut microbiota and acute CNS injuries. Experimental models identify a bidirectional communication between the gut and CNS in post-injury gut dysbiosis, intestinal lymphatic tissue-mediated neuroinflammation, and bacterial-metabolite-associated neurotransmission. Additionally, fecal microbiota transplantation, probiotics, and prebiotics manipulating the gut microbiota can be used as effective therapeutic agents to alleviate secondary brain injury and facilitate functional outcomes. The role of gut microbiota in acute CNS injury would be an exciting frontier in clinical and experimental medicine.
Highlights
Acute injuries to the central nervous system (CNS), such as stroke, traumatic brain injury (TBI), spinal cord injury (SCI), are critical global health problems that result in lifelong disabilities or death, leading to catastrophic changes to the injured individuals, alongside their family and even the entire community [1, 2]
We provide an update on the link between gut microbiota and acute CNS injuries
Gut microbiota is closely involved in the development and progression of acute CNS disease through multiple mechanisms, including immunological, endocrine, metabolic, and neural pathways
Summary
Acute injuries to the central nervous system (CNS), such as stroke, traumatic brain injury (TBI), spinal cord injury (SCI), are critical global health problems that result in lifelong disabilities or death, leading to catastrophic changes to the injured individuals, alongside their family and even the entire community [1, 2]. Microbial components and metabolites such as lipopolysaccharide (LPS), long-chain fatty acids (LCFAs), short-chain fatty acids (SCFAs), trimethylamine-N-oxide (TAMO), tryptophan, and polysaccharide A (PSA) are considered to induce neuroinflammation and modulate the function of CNS either directly or by activating migration of peripheral immune cells to the brain Gut microbiota affects the development and pathophysiology of the brain by immunological, endocrine, metabolic, and neural pathways Microbiomes and their metabolites could modulate the brain and behavior by affecting intestinal epithelial cells to alter gut barrier function, enteroendocrine cells to secret hormones, as well as dendritic cells and macrophage, to regulate immune and microglia activation.
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