Presentation Details
| Acute and chronic olfactory epithelial inflammation differentially impact the olfactory bulb, hippocampus, and cognitive function Derek C.Cox , Morning Dove Rose, Diego Rodriguez-Gil, Cuihong Jia. Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA |
Abstract
Olfactory epithelial (OE) inflammation disrupts the sense of smell and has been associated with cognitive dysfunction following viral infections such as COVID-19. Both acute and chronic inflammation damage olfactory sensory neurons in the OE, causing hyposmia/anosmia. However, the mechanism underlying olfactory epithelial inflammation-induced cognitive deficits is unknown. Using the methimazole-induced acute OE inflammation mouse model, we found that acute inflammation did not affect hippocampus-mediated spatial learning and memory function assessed by Barnes Maze test in both sexes. Although acute OE inflammation increased inflammatory cytokines, TNFα, IL-6 and IL-1β, as well as microglial activation and leukocyte infiltration, measured by CD68 and CD45, in the olfactory bulb of male mice, it did not induce inflammatory responses in the hippocampus of either sex. Using the inducible olfactory inflammation mouse model, we found that chronic OE inflammation reduced spatial learning and memory in both sexes. Chronic inflammation increased pro-inflammatory cytokines, microglial activation, and leukocyte infiltrations in the olfactory bulb of both sexes. Interestingly, 4 weeks after stopping chronic inflammation induction, when the OE is reconstituted and the smell function is restored, cognitive function was fully recovered in females but not in male mice, suggesting a sex difference in cognitive recovery following chronic OE inflammation-induced deficits. The hippocampal pathology during the chronic OE inflammation and recovery phases is under investigation. Together, these data suggest that acute and chronic OE inflammation differently affect cognitive function, and there might be an OE-OB-hippocampal inflammation pathway responsible for chronic OE inflammation-induced learning and memory deficits.
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