Poster abstracts
Poster number 94 submitted by Damon DiSabato
Social stress and the induction of neuronal IL-1b expression in the hippocampus activate microglia and cause the recruitment of leukocytes to the brain and spleen
Damon DiSabato (Neuroscience), Danny Nemeth (Biosciences), Xiaoyu Liu (Biosciences), Jonathan Godbout (Department of Neuroscience, College of Medicine), Ning Quan (Division of Biosciences, College of Dentistry)
Abstract:
Chronic stress is associated with an increased prevalence of mental health complications including anxiety and depression. We have previously reported that repeated social defeat (RSD) stress caused microglial activation, monocyte infiltration into brain, and robust IL-1 signaling. These neuroimmune effects with stress were associated with the induction of prolonged anxiety-like behavior. Thus, we hypothesize that IL-1 signaling in the brain with chronic stress plays a critical role in the regional-dependent recruitment of monocytes. Therefore, the role of central IL-1 signaling was examined by using adenoviral IL-1β (adIL-1β) administration into the ventral hippocampus (VH) in mice concomitantly subjected to a sub-threshold social defeat stress (STS) induced by paired fighting. This viral-mediated induction of IL-1β was primarily localized to hippocampal neurons. Mice were exposed 30 minutes of paired fighting for 6 consecutive days. This was a milder stress because these mice did not develop anxiety and showed no evidence of microglial activation. In addition, viral-mediated expression of IL-1β in the hippocampus alone activated microglia and increased leukocyte recruitment to the brain. This, however, did not increase leukocyte trafficking to the spleen to induce splenomegaly. The combination of the stress and viral-mediated expression of IL-1 in the hippocampus resulted in neuroinflammation and a significant increase in spleen size. Activated microglia and an increase in CD45+ infiltrating leukocytes were evident with a distinct localization within the dentate gyrus and hilus regions of the hippocampus, where IL-1β induction was prominent. Furthermore, this localization neuroinflammation was associated with a reduction in cellular density within the hippocampus. Taken together, these data indicate that neuronal IL-1 expression is a critical step in microglia activation and the subsequent recruitment of monocytes with a chronic stressor.
Keywords: Interleukin-1, Stress, Microglia