We have previously found that induction of brain TNFα following intraperitoneal injections of LPS, a toll-like receptor 4 agonist, is related to blood TNFα that is transported into the brain inducing a response that lasted at least 10 months [1]. We hypothesized that poly I:C, a TLR3 agonist known to activate systemic and brain innate immune responses, would induce parallel systemic and brain proinflammatory responses that cause persistent brain activation. Poly I:C treatment of mice increased TNFα serum levels that peak around three hours at more than tenfold basal levels returning to near zero by 24 hours (Figure 1). Poly I:C treatment increased brain levels of TNFα that peaked at three hours after poly I:C at about 6 fold basal levels and remained significantly elevated for at least three days. These findings are consistent with acute systemic proinflammatory activation contributing to persistent brain neuroinflammatory responses.
