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Traumatic brain injury (TBI)-induced cerebral inflammation involves several mediators including activation of resident microglia, infiltration of leukocytes, and release of proinflammatory cytokines and chemokines at the site of injury. Invading leukocytes, mainly neutrophil and inflammatory monocytes, contribute to ongoing post-TBI cerebral edema and neuronal injury. Based on the beneficial effect of ghrelin hormone treatment following TBI, we hypothesized that ghrelin may alter the infiltrating inflammatory cell profile.
Pubmed ID: 25494422
