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Lipopolysaccharide-induced apoptosis of olfactory receptor neurons in rats
Conclusion: Daily intranasal perfusion of lipopolysaccharide (LPS) for 14 days in rats induced apoptosis of olfactory receptor neurons (ORNs) over >3 but
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| Published in: | Acta oto-laryngologica 2007, Vol.127 (7), p.748-753 |
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| Main Authors: | , , , , , |
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| cited_by | cdi_FETCH-LOGICAL-c434t-8edf89a2c665771b1ed916d4a53798d78426495b246ee013c3dfc9e0a46d09473 |
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| cites | cdi_FETCH-LOGICAL-c434t-8edf89a2c665771b1ed916d4a53798d78426495b246ee013c3dfc9e0a46d09473 |
| container_end_page | 753 |
| container_issue | 7 |
| container_start_page | 748 |
| container_title | Acta oto-laryngologica |
| container_volume | 127 |
| creator | Yagi, Sayaka Tsukatani, Toshiaki Yata, Tsuyoshi Tsukioka, Fusae Miwa, Takaki Furukawa, Mitsuru |
| description | Conclusion: Daily intranasal perfusion of lipopolysaccharide (LPS) for 14 days in rats induced apoptosis of olfactory receptor neurons (ORNs) over >3 but |
| doi_str_mv | 10.1080/00016480601002062 |
| format | article |
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Objectives: 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. Materials and 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.</description><identifier>ISSN: 0001-6489</identifier><identifier>EISSN: 1651-2251</identifier><identifier>DOI: 10.1080/00016480601002062</identifier><identifier>PMID: 17573571</identifier><identifier>CODEN: AOLAAJ</identifier><language>eng</language><publisher>Stockholm: Informa UK Ltd</publisher><subject>Administration, Intranasal ; Animals ; Antibodies - immunology ; apoptosis ; Apoptosis - drug effects ; bcl-2-Associated X Protein - immunology ; bcl-2-Associated X Protein - metabolism ; Biological and medical sciences ; Caspase 3 - immunology ; Caspase 3 - metabolism ; DNA, Single-Stranded - immunology ; DNA, Single-Stranded - metabolism ; Escherichia coli ; Female ; Immunohistochemistry ; lipopolysaccharide ; Lipopolysaccharides - pharmacology ; Medical sciences ; Nasal Mucosa - metabolism ; olfactory receptor neurons ; Olfactory Receptor Neurons - pathology ; Otorhinolaryngology. Stomatology ; Proto-Oncogene Proteins c-bcl-2 - immunology ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Rats ; Rats, Sprague-Dawley</subject><ispartof>Acta oto-laryngologica, 2007, Vol.127 (7), p.748-753</ispartof><rights>2007 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2007</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-8edf89a2c665771b1ed916d4a53798d78426495b246ee013c3dfc9e0a46d09473</citedby><cites>FETCH-LOGICAL-c434t-8edf89a2c665771b1ed916d4a53798d78426495b246ee013c3dfc9e0a46d09473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18870251$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17573571$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yagi, Sayaka</creatorcontrib><creatorcontrib>Tsukatani, Toshiaki</creatorcontrib><creatorcontrib>Yata, Tsuyoshi</creatorcontrib><creatorcontrib>Tsukioka, Fusae</creatorcontrib><creatorcontrib>Miwa, Takaki</creatorcontrib><creatorcontrib>Furukawa, Mitsuru</creatorcontrib><title>Lipopolysaccharide-induced apoptosis of olfactory receptor neurons in rats</title><title>Acta oto-laryngologica</title><addtitle>Acta Otolaryngol</addtitle><description>Conclusion: Daily intranasal perfusion of lipopolysaccharide (LPS) for 14 days in rats induced apoptosis of olfactory receptor neurons (ORNs) over >3 but <7 days. Objectives: 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. Materials and 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.</description><subject>Administration, Intranasal</subject><subject>Animals</subject><subject>Antibodies - immunology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - immunology</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Biological and medical sciences</subject><subject>Caspase 3 - immunology</subject><subject>Caspase 3 - metabolism</subject><subject>DNA, Single-Stranded - immunology</subject><subject>DNA, Single-Stranded - metabolism</subject><subject>Escherichia coli</subject><subject>Female</subject><subject>Immunohistochemistry</subject><subject>lipopolysaccharide</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Medical sciences</subject><subject>Nasal Mucosa - metabolism</subject><subject>olfactory receptor neurons</subject><subject>Olfactory Receptor Neurons - pathology</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - immunology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>0001-6489</issn><issn>1651-2251</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNp9kE1r3DAQhkVpaLZJf0AvxZf25mZk65P0EkKatizkkpzNrDRmFbTWVrIJ--_rZTeEUMhJjOZ5h5mHsc8cvnMwcAEAXAkDCjhAA6p5xxZcSV43jeTv2WLfr2fAnrKPpTzuS2vkB3bKtdSt1HzB_izDNm1T3BV0bo05eKrD4CdHvsK5M6YSSpX6KsUe3ZjyrsrkaP7P1UBTTkOpwlBlHMs5O-kxFvp0fM_Yw8-b--tf9fLu9vf11bJ2ohVjbcj3xmLjlJJa8xUnb7nyAmWrrfHaiEYJK1eNUETAW9f63lkCFMqDFbo9Y98Oc7c5_Z2ojN0mFEcx4kBpKp0GaZWBPcgPoMuplEx9t81hg3nXcej2Arv_BM6ZL8fh02pD_iVxNDYDX48AFoexzzi4UF44YzTM9mfux4ELQ5_yBp9Sjr4bcRdTfg61b-1x-Sq-Jozj2mGm7jFNeZgFv3HFP4z-nRE</recordid><startdate>2007</startdate><enddate>2007</enddate><creator>Yagi, Sayaka</creator><creator>Tsukatani, Toshiaki</creator><creator>Yata, Tsuyoshi</creator><creator>Tsukioka, Fusae</creator><creator>Miwa, Takaki</creator><creator>Furukawa, Mitsuru</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><general>Taylor and Francis</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>8BM</scope></search><sort><creationdate>2007</creationdate><title>Lipopolysaccharide-induced apoptosis of olfactory receptor neurons in rats</title><author>Yagi, Sayaka ; Tsukatani, Toshiaki ; Yata, Tsuyoshi ; Tsukioka, Fusae ; Miwa, Takaki ; Furukawa, Mitsuru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-8edf89a2c665771b1ed916d4a53798d78426495b246ee013c3dfc9e0a46d09473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Administration, Intranasal</topic><topic>Animals</topic><topic>Antibodies - immunology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein - immunology</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Biological and medical sciences</topic><topic>Caspase 3 - immunology</topic><topic>Caspase 3 - metabolism</topic><topic>DNA, Single-Stranded - immunology</topic><topic>DNA, Single-Stranded - metabolism</topic><topic>Escherichia coli</topic><topic>Female</topic><topic>Immunohistochemistry</topic><topic>lipopolysaccharide</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Medical sciences</topic><topic>Nasal Mucosa - metabolism</topic><topic>olfactory receptor neurons</topic><topic>Olfactory Receptor Neurons - pathology</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - immunology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yagi, Sayaka</creatorcontrib><creatorcontrib>Tsukatani, Toshiaki</creatorcontrib><creatorcontrib>Yata, Tsuyoshi</creatorcontrib><creatorcontrib>Tsukioka, Fusae</creatorcontrib><creatorcontrib>Miwa, Takaki</creatorcontrib><creatorcontrib>Furukawa, Mitsuru</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>ComDisDome</collection><jtitle>Acta oto-laryngologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yagi, Sayaka</au><au>Tsukatani, Toshiaki</au><au>Yata, Tsuyoshi</au><au>Tsukioka, Fusae</au><au>Miwa, Takaki</au><au>Furukawa, Mitsuru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipopolysaccharide-induced apoptosis of olfactory receptor neurons in rats</atitle><jtitle>Acta oto-laryngologica</jtitle><addtitle>Acta Otolaryngol</addtitle><date>2007</date><risdate>2007</risdate><volume>127</volume><issue>7</issue><spage>748</spage><epage>753</epage><pages>748-753</pages><issn>0001-6489</issn><eissn>1651-2251</eissn><coden>AOLAAJ</coden><abstract>Conclusion: Daily intranasal perfusion of lipopolysaccharide (LPS) for 14 days in rats induced apoptosis of olfactory receptor neurons (ORNs) over >3 but <7 days. Objectives: 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. Materials and 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.</abstract><cop>Stockholm</cop><pub>Informa UK Ltd</pub><pmid>17573571</pmid><doi>10.1080/00016480601002062</doi><tpages>6</tpages></addata></record> |
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| ispartof | Acta oto-laryngologica, 2007, Vol.127 (7), p.748-753 |
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| language | eng |
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| source | Taylor and Francis:Jisc Collections:Taylor and Francis Read and Publish Agreement 2024-2025:Medical Collection (Reading list) |
| subjects | Administration, Intranasal Animals Antibodies - immunology apoptosis Apoptosis - drug effects bcl-2-Associated X Protein - immunology bcl-2-Associated X Protein - metabolism Biological and medical sciences Caspase 3 - immunology Caspase 3 - metabolism DNA, Single-Stranded - immunology DNA, Single-Stranded - metabolism Escherichia coli Female Immunohistochemistry lipopolysaccharide Lipopolysaccharides - pharmacology Medical sciences Nasal Mucosa - metabolism olfactory receptor neurons Olfactory Receptor Neurons - pathology Otorhinolaryngology. Stomatology Proto-Oncogene Proteins c-bcl-2 - immunology Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Rats, Sprague-Dawley |
| title | Lipopolysaccharide-induced apoptosis of olfactory receptor neurons in rats |
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