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Imaging of In Situ Interferon Gamma Production in the Mouse Spleen following Listeria monocytogenes Infection
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Interferon gamma causes olfactory dysfunction without concomitant neuroepithelial damage.

Tatyana Pozharskaya1, Andrew P Lane

  • 1Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD.

International Forum of Allergy & Rhinology
|October 10, 2013
PubMed
Summary
This summary is machine-generated.

Chronic interferon-gamma (IFN-γ) expression in mice reduced olfactory function without causing tissue damage. This suggests IFN-γ directly impacts olfactory neuron function, potentially explaining smell loss in chronic rhinosinusitis.

Keywords:
interferon gammaolfactory lossrhinosinusitistransgenic model

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Area of Science:

  • Immunology
  • Neuroscience
  • Otolaryngology

Background:

  • Olfactory loss is a common symptom of chronic rhinosinusitis (CRS).
  • Inflammatory processes in CRS can affect both conductive and sensorineural olfactory pathways.
  • Interferon-gamma (IFN-γ), a T helper 1 cytokine, is implicated in nonpolypoid CRS (CRSsNP) and sinonasal infections.

Purpose of the Study:

  • To investigate the effects of chronic IFN-γ expression on olfactory epithelium (OE) histology and function.
  • To elucidate the role of IFN-γ in inflammatory olfactory dysfunction.

Main Methods:

  • A transgenic mouse model was used to induce localized, temporally-controlled IFN-γ expression in the OE.
  • Olfactory tissue was analyzed using histology, immunohistochemistry, and electro-olfactography (EOG) after 6 weeks of IFN-γ expression.
  • Findings were compared to uninduced littermate controls.

Main Results:

  • Chronic IFN-γ expression did not alter the histological architecture of the olfactory neuroepithelium or lamina propria.
  • Electro-olfactography (EOG) revealed a significant decrease in odorant responses.
  • Increased submucosal CD45-positive cells, primarily CD3-positive and CD4-positive lymphocytes, were observed.

Conclusions:

  • Chronic IFN-γ expression in the OE diminishes odorant responsiveness despite the lack of apparent inflammatory tissue damage.
  • This suggests a direct functional effect of IFN-γ on olfactory neurons, potentially contributing to olfactory loss in CRSsNP and viral infections.
  • Submucosal lymphocyte infiltration indicates that other downstream cytokines may also play a role in olfactory dysfunction.