title: Lipopolysaccharide-induced apoptosis of olfactory receptor neurons in rats.
abstract: CONCLUSIONS
  Daily intranasal perfusion of lipopolysaccharide (LPS) for 14 days in rats induced apoptosis of olfactory receptor neurons (ORNs) over >3 but <7 days.
  
  
  OBJECTIVE
  Smoking is one of the factors causing olfactory dysfunction. LPS is a major glycolipid component of the gram-negative bacterial cell wall and an active component of cigarette smoke. We studied whether LPS is one of the causes of tobacco-induced olfactory dysfunction by examining apoptosis in the olfactory epithelium after local exposure to LPS.
  
  
  METHODS
  Rats received intranasal instillation of LPS or saline. Histochemical changes in the olfactory epithelium were examined using antibodies against single-stranded DNA, Bcl-2, Bax, and Caspase-3. We used different concentrations of LPS to examine the dose dependency and observed changes in the olfactory epithelium for a week after exposure cessation to see the duration of the effect of smoking.
  
  
  RESULTS
  We found that numbers of cells positive for ssDNA, Bcl-2, Bax, and Caspase-3 were increased on the exposed side. The number of ssDNA-positive cells reached a maximum on the first day and decreased to normal levels on the seventh day after cessation of exposure.
authors.affiliation: Department of Otorhinolaryngology, Head and Neck Surgery, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan. yagisajp@yahoo.co.jp
authors.forename: Sayaka
authors.initials: S
authors.lastname: Yagi
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Tsukatani
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Yata
authors.forename: Fusae
authors.initials: F
authors.lastname: Tsukioka
authors.forename: Takaki
authors.initials: T
authors.lastname: Miwa
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Furukawa
mesh_terms: D000281:Administration, Intranasal; D000818:Animals; D000906:Antibodies / Q000276:immunology; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000276:immunology / Q000378:metabolism; D004277:DNA, Single-Stranded / Q000276:immunology / Q000378:metabolism; D004926:Escherichia coli; D005260:Female; D007150:Immunohistochemistry; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009297:Nasal Mucosa / Q000378:metabolism; D018034:Olfactory Receptor Neurons / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000276:immunology / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051028:bcl-2-Associated X Protein / Q000276:immunology / Q000378:metabolism
chemical_list: D000906:Antibodies; C494826:BAX protein, human; D004277:DNA, Single-Stranded; D008070:Lipopolysaccharides; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D053148:Caspase 3