The TLR7 agonist imiquimod induces bronchodilation via a nonneuronal TLR7-independent mechanism: a possible role for quinoline in airway dilation.
Identifieur interne : 000210 ( PubMed/Corpus ); précédent : 000209; suivant : 000211The TLR7 agonist imiquimod induces bronchodilation via a nonneuronal TLR7-independent mechanism: a possible role for quinoline in airway dilation.
Auteurs : Olivia J. Larsson ; Martijn L. Manson ; Magnus Starkhammar ; Barbara Fuchs ; Mikael Adner ; Susanna Kumlien Georén ; Lars-Olaf CardellSource :
- American journal of physiology. Lung cellular and molecular physiology [ 1522-1504 ] ; 2016.
English descriptors
- KwdEn :
- Aminoquinolines (pharmacology), Animals, Asthma (drug therapy), Bronchioles (drug effects), Bronchioles (physiology), Bronchodilator Agents (pharmacology), Calcium Signaling, Cells, Cultured, Drug Evaluation, Preclinical, Guinea Pigs, Humans, Imiquimod, Male, Myocytes, Smooth Muscle (drug effects), Myocytes, Smooth Muscle (physiology), Toll-Like Receptor 7 (agonists).
- MESH :
- chemical , agonists : Toll-Like Receptor 7.
- chemical , pharmacology : Aminoquinolines, Bronchodilator Agents.
- drug effects : Bronchioles, Myocytes, Smooth Muscle.
- drug therapy : Asthma.
- physiology : Bronchioles, Myocytes, Smooth Muscle.
- Animals, Calcium Signaling, Cells, Cultured, Drug Evaluation, Preclinical, Guinea Pigs, Humans, Imiquimod, Male.
Abstract
Toll-like receptor (TLR) 7 agonists are known to reduce allergic airway inflammation. Their recently reported ability to rapidly relax airways has further increased their interest in the treatment of pulmonary disease. However, the mechanisms behind this effect are not fully understood. The present study, therefore, aimed to determine whether airway smooth muscle (ASM)-dependent mechanisms could be identified. TLR7 agonists were added to guinea pig airways following precontraction with carbachol in vitro or histamine in vivo. Pharmacological inhibitors were used to dissect conventional pathways of bronchodilation; tetrodotoxin was used or bilateral vagotomy was performed to assess neuronal involvement. Human ASM cells (HASMCs) were employed to determine the effect of TLR7 agonists on intracellular Ca(2+) ([Ca(2+)]i) mobilization. The well-established TLR7 agonist imiquimod rapidly relaxed precontracted airways in vitro and in vivo. This relaxation was demonstrated to be independent of nitric oxide, carbon monoxide, and cAMP signaling, as well as neuronal activity. A limited role for prostanoids could be detected. Imiquimod induced [Ca(2+)]i release from endoplasmic reticulum stores in HASMCs, inhibiting histamine-induced [Ca(2+)]i The TLR7 antagonist IRS661 failed to inhibit relaxation, and the structurally dissimilar agonist CL264 did not relax airways or inhibit [Ca(2+)]i This study shows that imiquimod acts directly on ASM to induce bronchorelaxation, via a TLR7-independent release of [Ca(2+)]i The effect is paralleled by other bronchorelaxant compounds, like chloroquine, which, like imiquimod, but unlike CL264, contains the chemical structure quinoline. Compounds with quinoline moieties may be of interest in the development of multifunctional drugs to treat pulmonary disease.
DOI: 10.1152/ajplung.00288.2015
PubMed: 27084847
Links to Exploration step
pubmed:27084847Le document en format XML
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Larsson</name><affiliation><nlm:affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden;</nlm:affiliation></affiliation></author><author><name sortKey="Manson, Martijn L" sort="Manson, Martijn L" uniqKey="Manson M" first="Martijn L" last="Manson">Martijn L. Manson</name><affiliation><nlm:affiliation>Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and Institute for Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Starkhammar, Magnus" sort="Starkhammar, Magnus" uniqKey="Starkhammar M" first="Magnus" last="Starkhammar">Magnus Starkhammar</name><affiliation><nlm:affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden; Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and.</nlm:affiliation></affiliation></author><author><name sortKey="Fuchs, Barbara" sort="Fuchs, Barbara" uniqKey="Fuchs B" first="Barbara" last="Fuchs">Barbara Fuchs</name><affiliation><nlm:affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden;</nlm:affiliation></affiliation></author><author><name sortKey="Adner, Mikael" sort="Adner, Mikael" uniqKey="Adner M" first="Mikael" last="Adner">Mikael Adner</name><affiliation><nlm:affiliation>Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and Institute for Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Kumlien Georen, Susanna" sort="Kumlien Georen, Susanna" uniqKey="Kumlien Georen S" first="Susanna" last="Kumlien Georén">Susanna Kumlien Georén</name><affiliation><nlm:affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden; Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and.</nlm:affiliation></affiliation></author><author><name sortKey="Cardell, Lars Olaf" sort="Cardell, Lars Olaf" uniqKey="Cardell L" first="Lars-Olaf" last="Cardell">Lars-Olaf Cardell</name><affiliation><nlm:affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden; Department of ENT Disease, Karolinska University Hospital, Stockholm, Sweden; lars-olaf.cardell@ki.se.</nlm:affiliation></affiliation></author></analytic><series><title level="j">American journal of physiology. Lung cellular and molecular physiology</title><idno type="eISSN">1522-1504</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aminoquinolines (pharmacology)</term><term>Animals</term><term>Asthma (drug therapy)</term><term>Bronchioles (drug effects)</term><term>Bronchioles (physiology)</term><term>Bronchodilator Agents (pharmacology)</term><term>Calcium Signaling</term><term>Cells, Cultured</term><term>Drug Evaluation, Preclinical</term><term>Guinea Pigs</term><term>Humans</term><term>Imiquimod</term><term>Male</term><term>Myocytes, Smooth Muscle (drug effects)</term><term>Myocytes, Smooth Muscle (physiology)</term><term>Toll-Like Receptor 7 (agonists)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Toll-Like Receptor 7</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aminoquinolines</term><term>Bronchodilator Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Bronchioles</term><term>Myocytes, Smooth Muscle</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Asthma</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Bronchioles</term><term>Myocytes, Smooth Muscle</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Calcium Signaling</term><term>Cells, Cultured</term><term>Drug Evaluation, Preclinical</term><term>Guinea Pigs</term><term>Humans</term><term>Imiquimod</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Toll-like receptor (TLR) 7 agonists are known to reduce allergic airway inflammation. Their recently reported ability to rapidly relax airways has further increased their interest in the treatment of pulmonary disease. However, the mechanisms behind this effect are not fully understood. The present study, therefore, aimed to determine whether airway smooth muscle (ASM)-dependent mechanisms could be identified. TLR7 agonists were added to guinea pig airways following precontraction with carbachol in vitro or histamine in vivo. Pharmacological inhibitors were used to dissect conventional pathways of bronchodilation; tetrodotoxin was used or bilateral vagotomy was performed to assess neuronal involvement. Human ASM cells (HASMCs) were employed to determine the effect of TLR7 agonists on intracellular Ca(2+) ([Ca(2+)]i) mobilization. The well-established TLR7 agonist imiquimod rapidly relaxed precontracted airways in vitro and in vivo. This relaxation was demonstrated to be independent of nitric oxide, carbon monoxide, and cAMP signaling, as well as neuronal activity. A limited role for prostanoids could be detected. Imiquimod induced [Ca(2+)]i release from endoplasmic reticulum stores in HASMCs, inhibiting histamine-induced [Ca(2+)]i The TLR7 antagonist IRS661 failed to inhibit relaxation, and the structurally dissimilar agonist CL264 did not relax airways or inhibit [Ca(2+)]i This study shows that imiquimod acts directly on ASM to induce bronchorelaxation, via a TLR7-independent release of [Ca(2+)]i The effect is paralleled by other bronchorelaxant compounds, like chloroquine, which, like imiquimod, but unlike CL264, contains the chemical structure quinoline. Compounds with quinoline moieties may be of interest in the development of multifunctional drugs to treat pulmonary disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27084847</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>15</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1504</ISSN><JournalIssue CitedMedium="Internet"><Volume>310</Volume><Issue>11</Issue><PubDate><Year>2016</Year><Month>06</Month><Day>01</Day></PubDate></JournalIssue><Title>American journal of physiology. Lung cellular and molecular physiology</Title><ISOAbbreviation>Am. J. Physiol. Lung Cell Mol. Physiol.</ISOAbbreviation></Journal><ArticleTitle>The TLR7 agonist imiquimod induces bronchodilation via a nonneuronal TLR7-independent mechanism: a possible role for quinoline in airway dilation.</ArticleTitle><Pagination><MedlinePgn>L1121-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajplung.00288.2015</ELocationID><Abstract><AbstractText>Toll-like receptor (TLR) 7 agonists are known to reduce allergic airway inflammation. Their recently reported ability to rapidly relax airways has further increased their interest in the treatment of pulmonary disease. However, the mechanisms behind this effect are not fully understood. The present study, therefore, aimed to determine whether airway smooth muscle (ASM)-dependent mechanisms could be identified. TLR7 agonists were added to guinea pig airways following precontraction with carbachol in vitro or histamine in vivo. Pharmacological inhibitors were used to dissect conventional pathways of bronchodilation; tetrodotoxin was used or bilateral vagotomy was performed to assess neuronal involvement. Human ASM cells (HASMCs) were employed to determine the effect of TLR7 agonists on intracellular Ca(2+) ([Ca(2+)]i) mobilization. The well-established TLR7 agonist imiquimod rapidly relaxed precontracted airways in vitro and in vivo. This relaxation was demonstrated to be independent of nitric oxide, carbon monoxide, and cAMP signaling, as well as neuronal activity. A limited role for prostanoids could be detected. Imiquimod induced [Ca(2+)]i release from endoplasmic reticulum stores in HASMCs, inhibiting histamine-induced [Ca(2+)]i The TLR7 antagonist IRS661 failed to inhibit relaxation, and the structurally dissimilar agonist CL264 did not relax airways or inhibit [Ca(2+)]i This study shows that imiquimod acts directly on ASM to induce bronchorelaxation, via a TLR7-independent release of [Ca(2+)]i The effect is paralleled by other bronchorelaxant compounds, like chloroquine, which, like imiquimod, but unlike CL264, contains the chemical structure quinoline. Compounds with quinoline moieties may be of interest in the development of multifunctional drugs to treat pulmonary disease.</AbstractText><CopyrightInformation>Copyright © 2016 the American Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Larsson</LastName><ForeName>Olivia J</ForeName><Initials>OJ</Initials><AffiliationInfo><Affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manson</LastName><ForeName>Martijn L</ForeName><Initials>ML</Initials><AffiliationInfo><Affiliation>Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and Institute for Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Starkhammar</LastName><ForeName>Magnus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden; Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fuchs</LastName><ForeName>Barbara</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Adner</LastName><ForeName>Mikael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and Institute for Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kumlien Georén</LastName><ForeName>Susanna</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden; Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cardell</LastName><ForeName>Lars-Olaf</ForeName><Initials>LO</Initials><AffiliationInfo><Affiliation>Division of ENT Diseases, CLINTEC, Karolinska Institutet, Stockholm, Sweden; Department of ENT Disease, Karolinska University Hospital, Stockholm, Sweden; lars-olaf.cardell@ki.se.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>04</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Lung Cell Mol Physiol</MedlineTA><NlmUniqueID>100901229</NlmUniqueID><ISSNLinking>1040-0605</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000634">Aminoquinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001993">Bronchodilator Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051199">Toll-Like Receptor 7</NameOfSubstance></Chemical><Chemical><RegistryNumber>P1QW714R7M</RegistryNumber><NameOfSubstance UI="D000077271">Imiquimod</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Am J Physiol Lung Cell Mol Physiol. 2016 Jul 1;311(1):L177</RefSource><PMID Version="1">27407079</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000634" MajorTopicYN="N">Aminoquinolines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001249" MajorTopicYN="N">Asthma</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055745" MajorTopicYN="N">Bronchioles</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001993" MajorTopicYN="N">Bronchodilator Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020013" MajorTopicYN="N">Calcium Signaling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004353" MajorTopicYN="N">Drug Evaluation, Preclinical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006168" MajorTopicYN="N">Guinea Pigs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077271" MajorTopicYN="N">Imiquimod</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D032389" MajorTopicYN="N">Myocytes, Smooth Muscle</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051199" MajorTopicYN="N">Toll-Like Receptor 7</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="Y">agonists</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">asthma</Keyword><Keyword MajorTopicYN="Y">bronchodilation</Keyword><Keyword MajorTopicYN="Y">imiquimod</Keyword><Keyword MajorTopicYN="Y">quinoline</Keyword><Keyword MajorTopicYN="Y">toll-like receptor 7</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>08</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>04</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>4</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>4</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>5</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27084847</ArticleId><ArticleId IdType="pii">ajplung.00288.2015</ArticleId><ArticleId IdType="doi">10.1152/ajplung.00288.2015</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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