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| Poster #254 Analyzing the Role of CD11b and Microglia in Recovery from Olfactory Injury |
| David Poore, Nick DeRusha, Diego Rodriguez-Gil East Tennessee State University, Johnson City, TN, United States |
Olfactory sensory neurons are constantly turning over; dead neurons are being engulfed and cleared, while newly differentiated neurons arise from stem cells. This neuroregeneration is facilitated by several cell types, including microglia and olfactory ensheathing cells. Here we focus on microglia, the immune cells of the CNS. Microglia show a robust response to injury and pathogens, moving towards the site of injury to respond through phagocytic and anti/pro-inflammatory pathways. Previously, our lab found an increase of integrin CD11b in the olfactory bulb (OB) following injury to the olfactory epithelium induced by a methimazole injection. We hypothesized microglia were directly involved in the recovery process in vivo and utilized CD11b-related pathways to respond and facilitate recovery. Using immunohistochemistry (IHC) and behavioral testing, motility of microglia throughout the OB and recovery from injury were analyzed by quantification of Iba1 expression and cell counts in the OB, along with the “Hidden Cookie” behavioral test, in both wild-type (WT) and CD11b-deficient knockout mice (CD11b-/-). For CD11b-/-, IHC experiments showed similar movement of microglia through the OB compared to WT, except at 7 days post-injury, which showed higher levels of Iba1 throughout the OBs. Additionally, behavioral data showed a slower functional recovery compared to WT, suggesting microglia’s involvement in the process in a time-dependent manner. Also, the differential pace of functional recovery for CD11b-/- mice supports that CD11b is directly involved, and further research is needed into the pathways at work. |