Spinal cord injury (SCI) disrupts the autonomic nervous system (ANS), impairing its ability to coordinate organ function throughout the body. Emerging data indicate that the systemic pathology that manifests from ANS dysfunction exacerbates intraspinal pathology and neurological impairment. Precisely how this happens is unknown, although new data, in both humans and in rodent models, implicate changes in the composition of bacteria in the gut (i.e., the gut microbiota) as disease-modifying factors that are capable of affecting systemic physiology and pathophysiology. Recent data from rodents indicate that SCI causes gut dysbiosis, which exacerbates intraspinal inflammation and lesion pathology leading to impaired recovery of motor function. Postinjury delivery of probiotics containing various types of "good" bacteria can partially overcome the pathophysiologal effects of gut dysbiosis; immune function, locomotor recovery, and spinal cord integrity are partially restored by a sustained regimen of oral probiotics. More research is needed to determine whether gut dysbiosis varies across a range of clinically relevant variables, including sex, injury level, and injury severity, and whether changes in the gut microbiota can predict the onset or severity of common postinjury comorbidities, including infection, anemia, metabolic syndrome, and, perhaps, secondary neurological deterioration. Those microbial populations that dominate the gut could become "druggable" targets that could be manipulated via dietary interventions. For example, personalized nutraceuticals (e.g., pre- or probiotics) could be developed to treat the above comorbidities and improve health and quality of life after SCI.
Keywords: Intestinal dysbiosis; Microbiome; Neuroinflammation; Probiotics; Spinal cord injury.