Presenter(s): Kelly Royster − Human Physiology
Faculty Mentor(s): Adrianne Huxtable, Austin Hocker
Poster 64
Research Area: Natural/Physical Science
Funding: Adrianne Huxtable’s Parker B. Francis Fellowship, University of Oregon
Inflammation is a component of all diseases, whereby key pro-inflammatory signaling molecules and receptors increase systemically and in the central nervous system (CNS). Systemic inflammation activates astrocytes and microglial cells in many regions of the CNS, which alter neuronal function and lead to behavioral changes. Our work has shown systemic inflammation impairs respiratory function through activation of the pro-inflammatory interleukin-1 receptors (IL-1RI) in the cervical spinal cord, but the roles of different cell types are unknown. To better understand how activation of IL-1RIs undermines breathing, we first need to determine what CNS cell types express IL-1RIs and how systemic inflammation changes IL-1RI expression. Based on the expression of IL-1RIs in other CNS regions, we hypothesized systemic inflammation would increase IL-1RI expression on identified neurons, astrocytes and microglia in the cervical spinal cord. Using immunohistochemistry to fluorescently label cell types and IL-1RIs, we first determined the optimal concentration of the IL-1RI antibody (1:250) by
a dilution series (n=5) in the hippocampus, where IL-1RI was known to be expressed after systemic inflammation. Further, preliminary data (n=2) suggest systemic inflammation increases IL-1RI expression on neurons (labeled by NeuN, 1:500) and astrocytes (labeled by GFAP, 1:500), but not microglia (labeled by Iba1, 1:1000). These results suggest neurons and astrocytes are likely the key cells undermining respiratory function after systemic inflammation. Understanding the mechanisms by which systemic inflammation undermines respiratory function may lead to targeted therapeutic interventions to promote breathing.