Journal
INTERNATIONAL FORUM OF ALLERGY & RHINOLOGY
Volume 8, Issue 3, Pages 415-420Publisher
WILEY
DOI: 10.1002/alr.22053
Keywords
chronic rhinosinusitis; inflammation; JNK; olfaction; olfactory disorders; olfactory sensory neurons
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Funding
- National Institutes of Health [DC009026]
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BackgroundOlfactory inflammation in chronic rhinosinusitis (CRS) is associated with cytokines that may result in the death of olfactory sensory neurons. The principal signaling molecules involved in the apoptotic pathway are c-Jun N-terminal kinases (JNK). Although the JNK pathway has emerged as a key player in programmed cell death in neuroinflammation, its specific role in CRS-associated olfactory loss has not been thoroughly investigated. MethodsJNK activation was studied in human tissue samples from 9 control and 11 CRS patients by immunohistochemical staining for phosphorylated c-Jun. A mouse model of inducible olfactory cytokine expression was used to experimentally control inflammation and assess JNK activation over time. ResultsIn patients with CRS, activation of c-Jun is significantly increased relative to non-CRS control subjects, and there is an associated loss of sensory neurons. In the olfactory inflammation mouse model, prolonged induction of inflammation results in elevation of c-Jun expression and neuronal apoptosis. ConclusionActivation of neuronal JNK is a feature of chronic olfactory inflammation that is associated with neuronal apoptosis. Given that inhibition of JNK activity is neuroprotective in other settings, antagonism of this pathway may have therapeutic potential in the management of inflammatory olfactory loss or other disorders linked to olfactory neuronal apoptosis.
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