Washington University in St. Louis (WU)
Our laboratory studies novel approaches to neuroprotection against secondary insults after traumatic brain injury (TBI). We have developed a mouse of model of delayed secondary systemic hypoxemia after TBI that models hypoxemia suffered by severe TBI patients in the intensive care unit. During the acute phase of TBI, patients are at high risk for infections, and are routinely exposed to antibiotics. Using this mouse model, we are studying the systemic secondary insults to antibiotic-induced gut microbial dysbiosis after TBI. We have found the neuroinflammatory response has an impact on injury and repair and long-term neurodegeneration and long-term behavior. We have demonstrated that the neuroinflammatory response and its sequelae after TBI are modifiable through gut microbiota modulation. We believe that a deeper understanding of the mechanisms by which TBI-associated neuroinflammation is modified by the enteric microbiome will generate the necessary foundation of knowledge to develop rationally-based strategies for neuroprotection.