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Cigarette Smoke-Induced Cell Death Causes Persistent Olfactory Dysfunction in Aged Mice.

Rumi Ueha1, Satoshi Ueha2, Kenji Kondo1

  • 1Department of Otolaryngology and Head and Neck Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Frontiers in Aging Neuroscience
|June 29, 2018
PubMed
Summary
This summary is machine-generated.

Cigarette smoke exposure damages olfactory receptor neurons (ORNs) in aged mice, leading to persistent olfactory dysfunction. Unlike in younger mice, ORN regeneration is impaired, suggesting a loss of regenerative capacity in older populations.

Keywords:
agingapoptosiscigarette smokinginflammatory cytokinesolfactory disfunctionolfactory epitheliumolfactory receptor neuron

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Area of Science:

  • Neuroscience
  • Toxicology
  • Gerontology

Background:

  • Cigarette smoke exposure is a known cause of olfactory dysfunction.
  • Previous studies showed olfactory receptor neuron (ORN) recovery in young mice after smoking cessation, but this is unclear in aged populations.

Purpose of the Study:

  • To investigate the effects of cigarette smoke on the olfactory receptor neuron (ORN) system in aged mice.
  • To determine the extent of ORN regeneration after smoking cessation in aged mice.

Main Methods:

  • Aged mice (16-month-old) were exposed to cigarette smoke solution (CSS) intranasally for 24 days.
  • Histological and gene analyses examined ORN survival, apoptosis, and inflammatory cytokines (TNF, Il6) in the olfactory epithelium (OE).
  • Olfactory function was assessed using habituation/dishabituation tests.

Main Results:

  • CSS exposure reduced mature ORN numbers and caused olfactory dysfunction in aged mice.
  • Apoptotic cell numbers increased, with elevated Tumor Necrosis Factor (TNF) and decreased Interleukin-6 (Il6) expression.
  • Olfactory dysfunction and reduced ORN numbers persisted even 28 days after cessation of CSS exposure.

Conclusions:

  • In aged mice, cigarette smoke exposure leads to increased ORN death.
  • The olfactory epithelium's regenerative capacity is overwhelmed, resulting in persistent olfactory dysfunction and reduced mature ORN numbers.