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Viral disruption of olfactory progenitors is exacerbated in allergic mice
R Ueha1, S Mukherjee2, S Ueha3
1Department of Pathology, University of Michigan, United States; Department of Otolaryngology, University of Tokyo, Japan.
Abstract:
Upper airway viral infection in patients with airway allergy often exacerbates olfactory dysfunction, but the mechanism for this exacerbation remains unclear. Here, we examined the effects of respiratory syncytial virus (RSV) infection, in the presence or absence of airway allergy, on olfactory receptor neurons (ORNs) and their progenitors in mice. Immunohistological analyses revealed that cockroach allergen (CRA)-induced airway allergy alone did not affect the number of OMP(+) mature ORNs and SOX2(+) ORN progenitors. Intranasal RSV line 19 infection in allergy-free mice resulted in a transient decrease in SOX2(+) ORN progenitors without affecting OMP(+) ORNs. In contrast, the RSV-induced decrease in SOX2(+) ORN progenitors was exacerbated and prolonged in allergic mice, which resulted in eventual loss of OMP(+) ORNs. In the allergic mice, reduction of RSV in the olfactory epithelium was delayed as compared with allergy-free mice. These results suggest that ORN progenitors were impaired by RSV infection and that airway allergy exacerbated damage to ORN progenitors by reducing viral clearance.
Insights
Airway allergy worsens olfactory dysfunction by impairing olfactory receptor neuron (ORN) progenitors during respiratory syncytial virus (RSV) infection. Allergy delays viral clearance, prolonging damage to these crucial sensory neurons.
Area of Science:
- Immunology
- Neuroscience
- Virology
Background:
- Upper airway viral infections can worsen olfactory dysfunction in individuals with airway allergies.
- The precise mechanisms underlying this exacerbation are not fully understood.
Purpose of the Study:
- To investigate the impact of respiratory syncytial virus (RSV) infection on olfactory receptor neurons (ORNs) and their progenitors in mice, with and without airway allergy.
- To elucidate the role of airway allergy in modulating the response to RSV infection in the olfactory epithelium.
Main Methods:
- Mice were subjected to cockroach allergen (CRA)-induced airway allergy and/or intranasal RSV line 19 infection.
- Immunohistological analyses were performed to quantify OMP(+) mature ORNs and SOX2(+) ORN progenitors.
- Viral load in the olfactory epithelium was assessed.
Main Results:
- Airway allergy alone did not alter the number of mature ORNs or ORN progenitors.
- RSV infection in non-allergic mice caused a temporary reduction in ORN progenitors but did not affect mature ORNs.
- In allergic mice, RSV infection led to a more severe and prolonged decrease in ORN progenitors, ultimately causing loss of mature ORNs.
- Viral clearance from the olfactory epithelium was delayed in allergic mice compared to non-allergic mice.
Conclusions:
- RSV infection impairs olfactory receptor neuron progenitors.
- Airway allergy exacerbates RSV-induced damage to ORN progenitors, likely by hindering viral clearance.
- These findings suggest a mechanism linking viral infections, allergy, and olfactory dysfunction.
