The Interaction Between Brain, Gut, & Microbiome and Implications Regarding Short and Long-term Recovery Post-Brain Injury

CHAIR

Lisa Brenner

PRESENTER

• Christopher Lowry
• Gerard Clarke

DESCRIPTION

Brain and systemic inflammation play a role in the vulnerability to, aggravation of, and perpetuation of adverse consequences of traumatic brain injury (TBI). Evidence suggests that elevations in proinflammatory markers, such as interleukin (IL)-6 and C-reactive protein (CRP), within the first 24 hours post-trauma, lead to worse outcomes post-TBI. Following acute TBI, cerebral inflammatory responses begin within minutes, and include elevations of IL-1β, IL-6, IL-8, and tumor necrosis factor alpha (TNFα). The increase in cerebral inflammatory response, including microglial and astroglial activation, is prolonged, lasting months or years, and contributes to the evolving symptomatology and pathology, thereby highlighting inflammation as a potential treatment target long after the acute trauma. TBI also induces secondary changes that lead to delayed neuroinflammation, neuronal cell death, impaired neurological function, and systemic inflammation. These inflammatory responses can also alter the human microbiome, reducing microbial diversity and potentially exacerbating physical and psychological symptoms.

LEARNING OBJECTIVES

• Brain-gut-microbiome axis regulation and dysregulation;
• Mechanisms of action of commensal bacteria on the nervous system and behavior in various models of neuroinflammation;
• “Old Friends Theory” and an immunization strategy for prevention of stress-related disorders (emotional/physical); and
• Study designs to facilitate exploration of the relationships between chronic inflammation, failing immunoregulation, and negative outcomes among those with a history of TBI (research implementing these designs is in progress).