Chronic olfactory inflammation: its impact on the olfactory epithelium, olfactory bulb and brain cognitive function
Abstract
Olfactory deficits positively correlate to cognitive dysfunction and are proposed as an early predictor for neurodegenerative diseases. Chronic olfactory inflammation following viral nose infection, including COVID-19, leads to loss of the sense of smell. Whether chronic olfactory inflammation impairs brain function, such as COVID-related cognition and memory decline, is not fully understood. Using an inducible olfactory inflammation (IOI) mouse model that induces TNFα expression under Cyp2g1, a marker for the olfactory epithelium (OE), we investigated the effect of chronic olfactory inflammation on OE, olfactory bulb (OB) and brain cognitive function. Six weeks after induction of TNFα, a massive inflammatory response was observed in the OE, including upregulation of IL-1β, IFNγ, IL-6, and CCL2. Olfactory sensory neurons were lost in a patchy pattern that matches the differential expression of Cyp2g1 in the OE. Basal stem cell proliferation was absent in injured and intact regions. Smell function, measured by buried food and olfactory habituation/dishabituation tests, was also impaired. In the OB, IOI elevated IL-1β and IL-6 mRNA, activated microglia and enhanced leukocyte infiltration. These data indicate that chronic OE inflammation disrupts the OE and its regenerative capacity, which then causes an inflammatory pathology in the OB. Importantly, hippocampus-mediated learning and memory, tested by Barnes maze and novel object recognition, was also compromised in the IOI mice. The IOI-induced hippocampal pathology is under investigation. Together, this study reveals an OE-OB-hippocampal pathway that might be correlated to cognitive decline following COVID-19-induced chronic olfactory inflammation.
Start Time
16-4-2025 1:30 PM
End Time
16-4-2025 4:00 PM
Presentation Type
Poster
Presentation Category
Science, Technology and Engineering
Student Type
Undergraduate Student
Faculty Mentor
Cuihong Jia
Faculty Department
Biomedical Sciences
Chronic olfactory inflammation: its impact on the olfactory epithelium, olfactory bulb and brain cognitive function
Olfactory deficits positively correlate to cognitive dysfunction and are proposed as an early predictor for neurodegenerative diseases. Chronic olfactory inflammation following viral nose infection, including COVID-19, leads to loss of the sense of smell. Whether chronic olfactory inflammation impairs brain function, such as COVID-related cognition and memory decline, is not fully understood. Using an inducible olfactory inflammation (IOI) mouse model that induces TNFα expression under Cyp2g1, a marker for the olfactory epithelium (OE), we investigated the effect of chronic olfactory inflammation on OE, olfactory bulb (OB) and brain cognitive function. Six weeks after induction of TNFα, a massive inflammatory response was observed in the OE, including upregulation of IL-1β, IFNγ, IL-6, and CCL2. Olfactory sensory neurons were lost in a patchy pattern that matches the differential expression of Cyp2g1 in the OE. Basal stem cell proliferation was absent in injured and intact regions. Smell function, measured by buried food and olfactory habituation/dishabituation tests, was also impaired. In the OB, IOI elevated IL-1β and IL-6 mRNA, activated microglia and enhanced leukocyte infiltration. These data indicate that chronic OE inflammation disrupts the OE and its regenerative capacity, which then causes an inflammatory pathology in the OB. Importantly, hippocampus-mediated learning and memory, tested by Barnes maze and novel object recognition, was also compromised in the IOI mice. The IOI-induced hippocampal pathology is under investigation. Together, this study reveals an OE-OB-hippocampal pathway that might be correlated to cognitive decline following COVID-19-induced chronic olfactory inflammation.