Eosinophil peroxidase induces the expression and function of acid-sensing ion channel-3 in allergic rhinitis: in vitro evidence in cultured epithelial cells

Summary Background Acid‐sensing ion channels (ASIC) are a family of acid‐activated ligand‐gated cation channels. As tissue acidosis is a feature of inflammatory conditions, such as allergic rhinitis (AR), we investigated the expression and function of these channels in AR. Objectives The aim of the...

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Veröffentlicht in:Clinical and experimental allergy 2012-07, Vol.42 (7), p.1028-1039
Hauptverfasser: G. Khoo, S., Al-Alawi, M., Walsh, M. T., Hennigan, K., Glynn, S., Thornton, M., McQuaid, S., Wang, Y., Hamilton, P. W., Verriere, V., Gleich, G. J., Harvey, B. J., Costello, R. W., McGarvey, L. P.
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container_end_page 1039
container_issue 7
container_start_page 1028
container_title Clinical and experimental allergy
container_volume 42
creator G. Khoo, S.
Al-Alawi, M.
Walsh, M. T.
Hennigan, K.
Glynn, S.
Thornton, M.
McQuaid, S.
Wang, Y.
Hamilton, P. W.
Verriere, V.
Gleich, G. J.
Harvey, B. J.
Costello, R. W.
McGarvey, L. P.
description Summary Background Acid‐sensing ion channels (ASIC) are a family of acid‐activated ligand‐gated cation channels. As tissue acidosis is a feature of inflammatory conditions, such as allergic rhinitis (AR), we investigated the expression and function of these channels in AR. Objectives The aim of the study was to assess expression and function of ASIC channels in the nasal mucosa of control and AR subjects. Methods Immunohistochemical localization of ASIC receptors and functional responses to lactic acid application were investigated. In vitro studies on cultured epithelial cells were performed to assess underlying mechanisms of ASIC function. Results Lactic acid at pH 7.03 induced a significant rise in nasal fluid secretion that was inhibited by pre‐treatment with the ASIC inhibitor amiloride in AR subjects (n = 19). Quantitative PCR on cDNA isolated from nasal biopsies from control and AR subjects demonstrated that ASIC‐1 was equally expressed in both populations, but ASIC‐3 was significantly more highly expressed in AR (P 
doi_str_mv 10.1111/j.1365-2222.2012.03980.x
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Khoo, S. ; Al-Alawi, M. ; Walsh, M. T. ; Hennigan, K. ; Glynn, S. ; Thornton, M. ; McQuaid, S. ; Wang, Y. ; Hamilton, P. W. ; Verriere, V. ; Gleich, G. J. ; Harvey, B. J. ; Costello, R. W. ; McGarvey, L. P.</creator><creatorcontrib>G. Khoo, S. ; Al-Alawi, M. ; Walsh, M. T. ; Hennigan, K. ; Glynn, S. ; Thornton, M. ; McQuaid, S. ; Wang, Y. ; Hamilton, P. W. ; Verriere, V. ; Gleich, G. J. ; Harvey, B. J. ; Costello, R. W. ; McGarvey, L. P.</creatorcontrib><description>Summary Background Acid‐sensing ion channels (ASIC) are a family of acid‐activated ligand‐gated cation channels. As tissue acidosis is a feature of inflammatory conditions, such as allergic rhinitis (AR), we investigated the expression and function of these channels in AR. Objectives The aim of the study was to assess expression and function of ASIC channels in the nasal mucosa of control and AR subjects. Methods Immunohistochemical localization of ASIC receptors and functional responses to lactic acid application were investigated. In vitro studies on cultured epithelial cells were performed to assess underlying mechanisms of ASIC function. Results Lactic acid at pH 7.03 induced a significant rise in nasal fluid secretion that was inhibited by pre‐treatment with the ASIC inhibitor amiloride in AR subjects (n = 19). Quantitative PCR on cDNA isolated from nasal biopsies from control and AR subjects demonstrated that ASIC‐1 was equally expressed in both populations, but ASIC‐3 was significantly more highly expressed in AR (P &lt; 0.02). Immunohistochemistry confirmed significantly higher ASIC‐3 protein expression on nasal epithelial cells in AR patients than controls (P &lt; 0.01). Immunoreactivity for EPO+ eosinophils in both nasal epithelium and submucosa was more prominent in AR compared with controls. A mechanism of induction of ASIC‐3 expression relevant to AR was suggested by the finding that eosinophil peroxidase (EPO), acting via ERK1/2, induced the expression of ASIC‐3 in epithelial cells. Furthermore, using a quantitative functional measure of epithelial cell secretory function in vitro, EPO increased the air‐surface liquid depth via an ASIC‐dependent chloride secretory pathway. Conclusions This data suggests a possible mechanism for the observed association of eosinophils and rhinorrhoea in AR and is manifested through enhanced ASIC‐3 expression.</description><identifier>ISSN: 0954-7894</identifier><identifier>EISSN: 1365-2222</identifier><identifier>DOI: 10.1111/j.1365-2222.2012.03980.x</identifier><identifier>PMID: 22702502</identifier><language>eng</language><publisher>Oxford: Blackwell Publishing Ltd</publisher><subject>Acid Sensing Ion Channels ; acid-activated ligand-gated cation channels ; Acidity ; Acidosis ; Adolescent ; Adult ; Allergic rhinitis ; Amiloride ; Biological and medical sciences ; Biopsy ; cation channels ; Cells, Cultured ; Chloride ; Data processing ; eosinophil ; Eosinophil Peroxidase - metabolism ; Epithelial cells ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Epithelium ; Extracellular signal-regulated kinase ; Female ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Gene Expression Regulation ; Humans ; Immunohistochemistry ; Inflammation ; Lactic acid ; Lactic Acid - pharmacology ; Leukocytes (eosinophilic) ; Male ; MAP Kinase Signaling System ; Medical sciences ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Mucosa ; Nasal Mucosa - metabolism ; Nasal Mucosa - pathology ; Non tumoral diseases ; Nose ; Otorhinolaryngology. Stomatology ; Peroxidase ; pH effects ; Polymerase Chain Reaction ; Rhinitis, Allergic, Seasonal - metabolism ; Rhinitis, Allergic, Seasonal - pathology ; Sodium channels ; Sodium Channels - biosynthesis ; Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</subject><ispartof>Clinical and experimental allergy, 2012-07, Vol.42 (7), p.1028-1039</ispartof><rights>2012 Blackwell Publishing Ltd</rights><rights>2015 INIST-CNRS</rights><rights>2012 Blackwell Publishing Ltd.</rights><rights>Copyright © 2012 Blackwell Publishing Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5640-ab42b7cc9c89f52fc8a601615724e94aaf9fc08b39b3e2f853ad93c628fb953d3</citedby><cites>FETCH-LOGICAL-c5640-ab42b7cc9c89f52fc8a601615724e94aaf9fc08b39b3e2f853ad93c628fb953d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2222.2012.03980.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2222.2012.03980.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=26016565$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22702502$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>G. Khoo, S.</creatorcontrib><creatorcontrib>Al-Alawi, M.</creatorcontrib><creatorcontrib>Walsh, M. T.</creatorcontrib><creatorcontrib>Hennigan, K.</creatorcontrib><creatorcontrib>Glynn, S.</creatorcontrib><creatorcontrib>Thornton, M.</creatorcontrib><creatorcontrib>McQuaid, S.</creatorcontrib><creatorcontrib>Wang, Y.</creatorcontrib><creatorcontrib>Hamilton, P. W.</creatorcontrib><creatorcontrib>Verriere, V.</creatorcontrib><creatorcontrib>Gleich, G. J.</creatorcontrib><creatorcontrib>Harvey, B. J.</creatorcontrib><creatorcontrib>Costello, R. W.</creatorcontrib><creatorcontrib>McGarvey, L. P.</creatorcontrib><title>Eosinophil peroxidase induces the expression and function of acid-sensing ion channel-3 in allergic rhinitis: in vitro evidence in cultured epithelial cells</title><title>Clinical and experimental allergy</title><addtitle>Clin Exp Allergy</addtitle><description>Summary Background Acid‐sensing ion channels (ASIC) are a family of acid‐activated ligand‐gated cation channels. As tissue acidosis is a feature of inflammatory conditions, such as allergic rhinitis (AR), we investigated the expression and function of these channels in AR. Objectives The aim of the study was to assess expression and function of ASIC channels in the nasal mucosa of control and AR subjects. Methods Immunohistochemical localization of ASIC receptors and functional responses to lactic acid application were investigated. In vitro studies on cultured epithelial cells were performed to assess underlying mechanisms of ASIC function. Results Lactic acid at pH 7.03 induced a significant rise in nasal fluid secretion that was inhibited by pre‐treatment with the ASIC inhibitor amiloride in AR subjects (n = 19). Quantitative PCR on cDNA isolated from nasal biopsies from control and AR subjects demonstrated that ASIC‐1 was equally expressed in both populations, but ASIC‐3 was significantly more highly expressed in AR (P &lt; 0.02). Immunohistochemistry confirmed significantly higher ASIC‐3 protein expression on nasal epithelial cells in AR patients than controls (P &lt; 0.01). Immunoreactivity for EPO+ eosinophils in both nasal epithelium and submucosa was more prominent in AR compared with controls. A mechanism of induction of ASIC‐3 expression relevant to AR was suggested by the finding that eosinophil peroxidase (EPO), acting via ERK1/2, induced the expression of ASIC‐3 in epithelial cells. Furthermore, using a quantitative functional measure of epithelial cell secretory function in vitro, EPO increased the air‐surface liquid depth via an ASIC‐dependent chloride secretory pathway. Conclusions This data suggests a possible mechanism for the observed association of eosinophils and rhinorrhoea in AR and is manifested through enhanced ASIC‐3 expression.</description><subject>Acid Sensing Ion Channels</subject><subject>acid-activated ligand-gated cation channels</subject><subject>Acidity</subject><subject>Acidosis</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Allergic rhinitis</subject><subject>Amiloride</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>cation channels</subject><subject>Cells, Cultured</subject><subject>Chloride</subject><subject>Data processing</subject><subject>eosinophil</subject><subject>Eosinophil Peroxidase - metabolism</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelium</subject><subject>Extracellular signal-regulated kinase</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Lactic acid</subject><subject>Lactic Acid - pharmacology</subject><subject>Leukocytes (eosinophilic)</subject><subject>Male</subject><subject>MAP Kinase Signaling System</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Mucosa</subject><subject>Nasal Mucosa - metabolism</subject><subject>Nasal Mucosa - pathology</subject><subject>Non tumoral diseases</subject><subject>Nose</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Peroxidase</subject><subject>pH effects</subject><subject>Polymerase Chain Reaction</subject><subject>Rhinitis, Allergic, Seasonal - metabolism</subject><subject>Rhinitis, Allergic, Seasonal - pathology</subject><subject>Sodium channels</subject><subject>Sodium Channels - biosynthesis</subject><subject>Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</subject><issn>0954-7894</issn><issn>1365-2222</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUd1u0zAUthCIlcIrIEsIiZsUx46TGImLqeo2pKlc8LNLy3FOVhfXyexkdO_Cw2LTUiSudm5sH38_x_4QwjlZ5LHebxc5K3lGYy0oyemCMFGTxf4Jmp0unqIZEbzIqloUZ-hFCFtCCOOifo7OKK0I5YTO0K9VH4zrh42xeADf702rAmDj2klDwOMGMOwHDyGY3mHlWtxNTo_p0HdYadNmAVyUuMWppzfKObAZiwpYWQv-1mjsN8aZ0YQPqXtvRt9juDctOJ2csJ7sOHloMQwmGlqjLNZgbXiJnnXKBnh1XOfo28Xq6_Iqu_58-Wl5fp1pXhYkU01Bm0proWvRcdrpWpUkL3Ne0QJEoVQnOk3qhomGAe1qzlQrmC5p3TWCs5bN0buD7uD7uwnCKHcmpAmUg34KMie0KMtCCPoYaJ5TzqLJHL35D7rtJ-_iQ2TOqYjfT8okWB9Q2vcheOjk4M1O-YcoJVPYcitTpjJlKlPY8k_Ych-pr48GU7OD9kT8m24EvD0CVNDKdl45bcI_XPolXqZJPx5wP42Fh0cPIJer87SL_OzAN2GE_Ymv_A9ZVqzi8mZ9KS_Wy_XNl-9XUew38ujV4A</recordid><startdate>201207</startdate><enddate>201207</enddate><creator>G. Khoo, S.</creator><creator>Al-Alawi, M.</creator><creator>Walsh, M. T.</creator><creator>Hennigan, K.</creator><creator>Glynn, S.</creator><creator>Thornton, M.</creator><creator>McQuaid, S.</creator><creator>Wang, Y.</creator><creator>Hamilton, P. W.</creator><creator>Verriere, V.</creator><creator>Gleich, G. J.</creator><creator>Harvey, B. J.</creator><creator>Costello, R. W.</creator><creator>McGarvey, L. P.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201207</creationdate><title>Eosinophil peroxidase induces the expression and function of acid-sensing ion channel-3 in allergic rhinitis: in vitro evidence in cultured epithelial cells</title><author>G. Khoo, S. ; Al-Alawi, M. ; Walsh, M. T. ; Hennigan, K. ; Glynn, S. ; Thornton, M. ; McQuaid, S. ; Wang, Y. ; Hamilton, P. W. ; Verriere, V. ; Gleich, G. J. ; Harvey, B. J. ; Costello, R. W. ; McGarvey, L. P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5640-ab42b7cc9c89f52fc8a601615724e94aaf9fc08b39b3e2f853ad93c628fb953d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acid Sensing Ion Channels</topic><topic>acid-activated ligand-gated cation channels</topic><topic>Acidity</topic><topic>Acidosis</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Allergic rhinitis</topic><topic>Amiloride</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>cation channels</topic><topic>Cells, Cultured</topic><topic>Chloride</topic><topic>Data processing</topic><topic>eosinophil</topic><topic>Eosinophil Peroxidase - metabolism</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelium</topic><topic>Extracellular signal-regulated kinase</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Lactic acid</topic><topic>Lactic Acid - pharmacology</topic><topic>Leukocytes (eosinophilic)</topic><topic>Male</topic><topic>MAP Kinase Signaling System</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Mucosa</topic><topic>Nasal Mucosa - metabolism</topic><topic>Nasal Mucosa - pathology</topic><topic>Non tumoral diseases</topic><topic>Nose</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Peroxidase</topic><topic>pH effects</topic><topic>Polymerase Chain Reaction</topic><topic>Rhinitis, Allergic, Seasonal - metabolism</topic><topic>Rhinitis, Allergic, Seasonal - pathology</topic><topic>Sodium channels</topic><topic>Sodium Channels - biosynthesis</topic><topic>Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>G. Khoo, S.</creatorcontrib><creatorcontrib>Al-Alawi, M.</creatorcontrib><creatorcontrib>Walsh, M. T.</creatorcontrib><creatorcontrib>Hennigan, K.</creatorcontrib><creatorcontrib>Glynn, S.</creatorcontrib><creatorcontrib>Thornton, M.</creatorcontrib><creatorcontrib>McQuaid, S.</creatorcontrib><creatorcontrib>Wang, Y.</creatorcontrib><creatorcontrib>Hamilton, P. W.</creatorcontrib><creatorcontrib>Verriere, V.</creatorcontrib><creatorcontrib>Gleich, G. J.</creatorcontrib><creatorcontrib>Harvey, B. J.</creatorcontrib><creatorcontrib>Costello, R. W.</creatorcontrib><creatorcontrib>McGarvey, L. P.</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental allergy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>G. Khoo, S.</au><au>Al-Alawi, M.</au><au>Walsh, M. T.</au><au>Hennigan, K.</au><au>Glynn, S.</au><au>Thornton, M.</au><au>McQuaid, S.</au><au>Wang, Y.</au><au>Hamilton, P. W.</au><au>Verriere, V.</au><au>Gleich, G. J.</au><au>Harvey, B. J.</au><au>Costello, R. W.</au><au>McGarvey, L. P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Eosinophil peroxidase induces the expression and function of acid-sensing ion channel-3 in allergic rhinitis: in vitro evidence in cultured epithelial cells</atitle><jtitle>Clinical and experimental allergy</jtitle><addtitle>Clin Exp Allergy</addtitle><date>2012-07</date><risdate>2012</risdate><volume>42</volume><issue>7</issue><spage>1028</spage><epage>1039</epage><pages>1028-1039</pages><issn>0954-7894</issn><eissn>1365-2222</eissn><abstract>Summary Background Acid‐sensing ion channels (ASIC) are a family of acid‐activated ligand‐gated cation channels. As tissue acidosis is a feature of inflammatory conditions, such as allergic rhinitis (AR), we investigated the expression and function of these channels in AR. Objectives The aim of the study was to assess expression and function of ASIC channels in the nasal mucosa of control and AR subjects. Methods Immunohistochemical localization of ASIC receptors and functional responses to lactic acid application were investigated. In vitro studies on cultured epithelial cells were performed to assess underlying mechanisms of ASIC function. Results Lactic acid at pH 7.03 induced a significant rise in nasal fluid secretion that was inhibited by pre‐treatment with the ASIC inhibitor amiloride in AR subjects (n = 19). Quantitative PCR on cDNA isolated from nasal biopsies from control and AR subjects demonstrated that ASIC‐1 was equally expressed in both populations, but ASIC‐3 was significantly more highly expressed in AR (P &lt; 0.02). Immunohistochemistry confirmed significantly higher ASIC‐3 protein expression on nasal epithelial cells in AR patients than controls (P &lt; 0.01). Immunoreactivity for EPO+ eosinophils in both nasal epithelium and submucosa was more prominent in AR compared with controls. A mechanism of induction of ASIC‐3 expression relevant to AR was suggested by the finding that eosinophil peroxidase (EPO), acting via ERK1/2, induced the expression of ASIC‐3 in epithelial cells. Furthermore, using a quantitative functional measure of epithelial cell secretory function in vitro, EPO increased the air‐surface liquid depth via an ASIC‐dependent chloride secretory pathway. Conclusions This data suggests a possible mechanism for the observed association of eosinophils and rhinorrhoea in AR and is manifested through enhanced ASIC‐3 expression.</abstract><cop>Oxford</cop><pub>Blackwell Publishing Ltd</pub><pmid>22702502</pmid><doi>10.1111/j.1365-2222.2012.03980.x</doi><tpages>12</tpages></addata></record>
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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Acid Sensing Ion Channels
acid-activated ligand-gated cation channels
Acidity
Acidosis
Adolescent
Adult
Allergic rhinitis
Amiloride
Biological and medical sciences
Biopsy
cation channels
Cells, Cultured
Chloride
Data processing
eosinophil
Eosinophil Peroxidase - metabolism
Epithelial cells
Epithelial Cells - metabolism
Epithelial Cells - pathology
Epithelium
Extracellular signal-regulated kinase
Female
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Gene Expression Regulation
Humans
Immunohistochemistry
Inflammation
Lactic acid
Lactic Acid - pharmacology
Leukocytes (eosinophilic)
Male
MAP Kinase Signaling System
Medical sciences
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Mucosa
Nasal Mucosa - metabolism
Nasal Mucosa - pathology
Non tumoral diseases
Nose
Otorhinolaryngology. Stomatology
Peroxidase
pH effects
Polymerase Chain Reaction
Rhinitis, Allergic, Seasonal - metabolism
Rhinitis, Allergic, Seasonal - pathology
Sodium channels
Sodium Channels - biosynthesis
Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology
title Eosinophil peroxidase induces the expression and function of acid-sensing ion channel-3 in allergic rhinitis: in vitro evidence in cultured epithelial cells
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