Pathology of the olfactory epithelium

Smoking and ethanol exposure

J. Vent, A. M. Robinson, M. J. Gentry-Nielsen, D. B. Conley, Richard J. Hallworth, D. A. Leopold, R. C. Kern

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Objective: To investigate the effects of tobacco smoke on the olfactory epithelium. Cigarette smoking has been associated with hyposmia; however, the pathophysiology is poorly understood. The sense of smell is mediated by olfactory sensory neurons (OSNs) exposed to the nasal airway, rendering them vulnerable to environmental injury and death. As a consequence, a baseline level of apoptotic OSN death has been demonstrated even in the absence of obvious disease. Dead OSNs are replaced by the mitosis and maturation of progenitors to maintain sufficient numbers of neurons into adult life. Disruption of this balance has been suggested as a common cause for clinical smell loss. This current study will evaluate the effects of tobacco smoke on the olfactory mucosa, with emphasis on changes in the degree of OSN apoptosis. Study Design: A rat model was used to assess the olfactory epithelium after exposure to tobacco smoke. Methods: Rats were exposed to tobacco smoke alone (for 12 weeks), smoke plus dietary ethanol (for the final 5 weeks), or to neither (control). Immunohistochemical analysis of the olfactory epithelium was performed using an antibody to the active form of caspase-3. Positive staining for this form of the caspase-3 enzyme indicates a cell undergoing apoptotic proteolysis. Results: Control rats demonstrated a low baseline level of caspase-3 activity in the olfactory epithelium. In contrast, tobacco smoke exposure triggered a dramatic increase in the degree of OSN apoptosis that affected all stages of the neuronal lineage. Conclusions: These results support the following hypothesis: smell loss in smokers is triggered by increased OSN death, which eventually overwhelms the regenerative capacity of the epithelium.

Original languageEnglish
Pages (from-to)1383-1388
Number of pages6
JournalLaryngoscope
Volume114
Issue number8 I
DOIs
StatePublished - Aug 2004

Fingerprint

Olfactory Receptor Neurons
Olfactory Mucosa
Smoke
Ethanol
Smoking
Tobacco
Pathology
Smell
Caspase 3
Apoptosis
Nose
Mitosis
Proteolysis
Epithelium
Staining and Labeling
Neurons
Antibodies
Wounds and Injuries
Enzymes

All Science Journal Classification (ASJC) codes

  • Otorhinolaryngology

Cite this

Vent, J., Robinson, A. M., Gentry-Nielsen, M. J., Conley, D. B., Hallworth, R. J., Leopold, D. A., & Kern, R. C. (2004). Pathology of the olfactory epithelium: Smoking and ethanol exposure. Laryngoscope, 114(8 I), 1383-1388. https://doi.org/10.1097/00005537-200408000-00012

Pathology of the olfactory epithelium : Smoking and ethanol exposure. / Vent, J.; Robinson, A. M.; Gentry-Nielsen, M. J.; Conley, D. B.; Hallworth, Richard J.; Leopold, D. A.; Kern, R. C.

In: Laryngoscope, Vol. 114, No. 8 I, 08.2004, p. 1383-1388.

Research output: Contribution to journalArticle

Vent, J, Robinson, AM, Gentry-Nielsen, MJ, Conley, DB, Hallworth, RJ, Leopold, DA & Kern, RC 2004, 'Pathology of the olfactory epithelium: Smoking and ethanol exposure', Laryngoscope, vol. 114, no. 8 I, pp. 1383-1388. https://doi.org/10.1097/00005537-200408000-00012
Vent J, Robinson AM, Gentry-Nielsen MJ, Conley DB, Hallworth RJ, Leopold DA et al. Pathology of the olfactory epithelium: Smoking and ethanol exposure. Laryngoscope. 2004 Aug;114(8 I):1383-1388. https://doi.org/10.1097/00005537-200408000-00012
Vent, J. ; Robinson, A. M. ; Gentry-Nielsen, M. J. ; Conley, D. B. ; Hallworth, Richard J. ; Leopold, D. A. ; Kern, R. C. / Pathology of the olfactory epithelium : Smoking and ethanol exposure. In: Laryngoscope. 2004 ; Vol. 114, No. 8 I. pp. 1383-1388.
@article{9949e6d20b574ff9b08dc71985953b00,
title = "Pathology of the olfactory epithelium: Smoking and ethanol exposure",
abstract = "Objective: To investigate the effects of tobacco smoke on the olfactory epithelium. Cigarette smoking has been associated with hyposmia; however, the pathophysiology is poorly understood. The sense of smell is mediated by olfactory sensory neurons (OSNs) exposed to the nasal airway, rendering them vulnerable to environmental injury and death. As a consequence, a baseline level of apoptotic OSN death has been demonstrated even in the absence of obvious disease. Dead OSNs are replaced by the mitosis and maturation of progenitors to maintain sufficient numbers of neurons into adult life. Disruption of this balance has been suggested as a common cause for clinical smell loss. This current study will evaluate the effects of tobacco smoke on the olfactory mucosa, with emphasis on changes in the degree of OSN apoptosis. Study Design: A rat model was used to assess the olfactory epithelium after exposure to tobacco smoke. Methods: Rats were exposed to tobacco smoke alone (for 12 weeks), smoke plus dietary ethanol (for the final 5 weeks), or to neither (control). Immunohistochemical analysis of the olfactory epithelium was performed using an antibody to the active form of caspase-3. Positive staining for this form of the caspase-3 enzyme indicates a cell undergoing apoptotic proteolysis. Results: Control rats demonstrated a low baseline level of caspase-3 activity in the olfactory epithelium. In contrast, tobacco smoke exposure triggered a dramatic increase in the degree of OSN apoptosis that affected all stages of the neuronal lineage. Conclusions: These results support the following hypothesis: smell loss in smokers is triggered by increased OSN death, which eventually overwhelms the regenerative capacity of the epithelium.",
author = "J. Vent and Robinson, {A. M.} and Gentry-Nielsen, {M. J.} and Conley, {D. B.} and Hallworth, {Richard J.} and Leopold, {D. A.} and Kern, {R. C.}",
year = "2004",
month = "8",
doi = "10.1097/00005537-200408000-00012",
language = "English",
volume = "114",
pages = "1383--1388",
journal = "Laryngoscope",
issn = "0023-852X",
publisher = "John Wiley and Sons Inc.",
number = "8 I",

}

TY - JOUR

T1 - Pathology of the olfactory epithelium

T2 - Smoking and ethanol exposure

AU - Vent, J.

AU - Robinson, A. M.

AU - Gentry-Nielsen, M. J.

AU - Conley, D. B.

AU - Hallworth, Richard J.

AU - Leopold, D. A.

AU - Kern, R. C.

PY - 2004/8

Y1 - 2004/8

N2 - Objective: To investigate the effects of tobacco smoke on the olfactory epithelium. Cigarette smoking has been associated with hyposmia; however, the pathophysiology is poorly understood. The sense of smell is mediated by olfactory sensory neurons (OSNs) exposed to the nasal airway, rendering them vulnerable to environmental injury and death. As a consequence, a baseline level of apoptotic OSN death has been demonstrated even in the absence of obvious disease. Dead OSNs are replaced by the mitosis and maturation of progenitors to maintain sufficient numbers of neurons into adult life. Disruption of this balance has been suggested as a common cause for clinical smell loss. This current study will evaluate the effects of tobacco smoke on the olfactory mucosa, with emphasis on changes in the degree of OSN apoptosis. Study Design: A rat model was used to assess the olfactory epithelium after exposure to tobacco smoke. Methods: Rats were exposed to tobacco smoke alone (for 12 weeks), smoke plus dietary ethanol (for the final 5 weeks), or to neither (control). Immunohistochemical analysis of the olfactory epithelium was performed using an antibody to the active form of caspase-3. Positive staining for this form of the caspase-3 enzyme indicates a cell undergoing apoptotic proteolysis. Results: Control rats demonstrated a low baseline level of caspase-3 activity in the olfactory epithelium. In contrast, tobacco smoke exposure triggered a dramatic increase in the degree of OSN apoptosis that affected all stages of the neuronal lineage. Conclusions: These results support the following hypothesis: smell loss in smokers is triggered by increased OSN death, which eventually overwhelms the regenerative capacity of the epithelium.

AB - Objective: To investigate the effects of tobacco smoke on the olfactory epithelium. Cigarette smoking has been associated with hyposmia; however, the pathophysiology is poorly understood. The sense of smell is mediated by olfactory sensory neurons (OSNs) exposed to the nasal airway, rendering them vulnerable to environmental injury and death. As a consequence, a baseline level of apoptotic OSN death has been demonstrated even in the absence of obvious disease. Dead OSNs are replaced by the mitosis and maturation of progenitors to maintain sufficient numbers of neurons into adult life. Disruption of this balance has been suggested as a common cause for clinical smell loss. This current study will evaluate the effects of tobacco smoke on the olfactory mucosa, with emphasis on changes in the degree of OSN apoptosis. Study Design: A rat model was used to assess the olfactory epithelium after exposure to tobacco smoke. Methods: Rats were exposed to tobacco smoke alone (for 12 weeks), smoke plus dietary ethanol (for the final 5 weeks), or to neither (control). Immunohistochemical analysis of the olfactory epithelium was performed using an antibody to the active form of caspase-3. Positive staining for this form of the caspase-3 enzyme indicates a cell undergoing apoptotic proteolysis. Results: Control rats demonstrated a low baseline level of caspase-3 activity in the olfactory epithelium. In contrast, tobacco smoke exposure triggered a dramatic increase in the degree of OSN apoptosis that affected all stages of the neuronal lineage. Conclusions: These results support the following hypothesis: smell loss in smokers is triggered by increased OSN death, which eventually overwhelms the regenerative capacity of the epithelium.

UR - http://www.scopus.com/inward/record.url?scp=3242679356&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=3242679356&partnerID=8YFLogxK

U2 - 10.1097/00005537-200408000-00012

DO - 10.1097/00005537-200408000-00012

M3 - Article

VL - 114

SP - 1383

EP - 1388

JO - Laryngoscope

JF - Laryngoscope

SN - 0023-852X

IS - 8 I

ER -