Differential requirement for c-Jun N-terminal kinase 1 in lung inflammation and host defense.
Identifieur interne : 000575 ( PubMed/Corpus ); précédent : 000574; suivant : 000576Differential requirement for c-Jun N-terminal kinase 1 in lung inflammation and host defense.
Auteurs : Jos Van Der Velden ; Yvonne M W. Janssen-Heininger ; Sivanarayna Mandalapu ; Erich V. Scheller ; Jay K. Kolls ; John F. AlcornSource :
- PloS one [ 1932-6203 ] ; 2012.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Interleukin-17, Mitogen-Activated Protein Kinase 8.
- immunology : Lung.
- metabolism : Lung, Pneumonia.
- microbiology : Lung.
- pathogenicity : Staphylococcus aureus.
- physiology : Signal Transduction.
- Animals, Cells, Cultured, Mice, Mice, Knockout.
Abstract
The c-Jun N-terminal kinase (JNK) - 1 pathway has been implicated in the cellular response to stress in many tissues and models. JNK1 is known to play a role in a variety of signaling cascades, including those involved in lung disease pathogenesis. Recently, a role for JNK1 signaling in immune cell function has emerged. The goal of the present study was to determine the role of JNK1 in host defense against both bacterial and viral pneumonia, as well as the impact of JNK1 signaling on IL-17 mediated immunity. Wild type (WT) and JNK1 -/- mice were challenged with Escherichia coli, Staphylococcus aureus, or Influenza A. In addition, WT and JNK1 -/- mice and epithelial cells were stimulated with IL-17A. The impact of JNK1 deletion on pathogen clearance, inflammation, and histopathology was assessed. JNK1 was required for clearance of E. coli, inflammatory cell recruitment, and cytokine production. Interestingly, JNK1 deletion had only a small impact on the host response to S. aureus. JNK1 -/- mice had decreased Influenza A burden in viral pneumonia, yet displayed worsened morbidity. Finally, JNK1 was required for IL-17A mediated induction of inflammatory cytokines and antimicrobial peptides both in epithelial cells and the lung. These data identify JNK1 as an important signaling molecule in host defense and demonstrate a pathogen specific role in disease. Manipulation of the JNK1 pathway may represent a novel therapeutic target in pneumonia.
DOI: 10.1371/journal.pone.0034638
PubMed: 22514650
Links to Exploration step
pubmed:22514650Le document en format XML
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Janssen-Heininger</name></author><author><name sortKey="Mandalapu, Sivanarayna" sort="Mandalapu, Sivanarayna" uniqKey="Mandalapu S" first="Sivanarayna" last="Mandalapu">Sivanarayna Mandalapu</name></author><author><name sortKey="Scheller, Erich V" sort="Scheller, Erich V" uniqKey="Scheller E" first="Erich V" last="Scheller">Erich V. Scheller</name></author><author><name sortKey="Kolls, Jay K" sort="Kolls, Jay K" uniqKey="Kolls J" first="Jay K" last="Kolls">Jay K. Kolls</name></author><author><name sortKey="Alcorn, John F" sort="Alcorn, John F" uniqKey="Alcorn J" first="John F" last="Alcorn">John F. 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Janssen-Heininger</name></author><author><name sortKey="Mandalapu, Sivanarayna" sort="Mandalapu, Sivanarayna" uniqKey="Mandalapu S" first="Sivanarayna" last="Mandalapu">Sivanarayna Mandalapu</name></author><author><name sortKey="Scheller, Erich V" sort="Scheller, Erich V" uniqKey="Scheller E" first="Erich V" last="Scheller">Erich V. Scheller</name></author><author><name sortKey="Kolls, Jay K" sort="Kolls, Jay K" uniqKey="Kolls J" first="Jay K" last="Kolls">Jay K. Kolls</name></author><author><name sortKey="Alcorn, John F" sort="Alcorn, John F" uniqKey="Alcorn J" first="John F" last="Alcorn">John F. Alcorn</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Interleukin-17 (metabolism)</term><term>Lung (immunology)</term><term>Lung (metabolism)</term><term>Lung (microbiology)</term><term>Mice</term><term>Mice, Knockout</term><term>Mitogen-Activated Protein Kinase 8 (metabolism)</term><term>Pneumonia (metabolism)</term><term>Signal Transduction (physiology)</term><term>Staphylococcus aureus (pathogenicity)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interleukin-17</term><term>Mitogen-Activated Protein Kinase 8</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Staphylococcus aureus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The c-Jun N-terminal kinase (JNK) - 1 pathway has been implicated in the cellular response to stress in many tissues and models. JNK1 is known to play a role in a variety of signaling cascades, including those involved in lung disease pathogenesis. Recently, a role for JNK1 signaling in immune cell function has emerged. The goal of the present study was to determine the role of JNK1 in host defense against both bacterial and viral pneumonia, as well as the impact of JNK1 signaling on IL-17 mediated immunity. Wild type (WT) and JNK1 -/- mice were challenged with Escherichia coli, Staphylococcus aureus, or Influenza A. In addition, WT and JNK1 -/- mice and epithelial cells were stimulated with IL-17A. The impact of JNK1 deletion on pathogen clearance, inflammation, and histopathology was assessed. JNK1 was required for clearance of E. coli, inflammatory cell recruitment, and cytokine production. Interestingly, JNK1 deletion had only a small impact on the host response to S. aureus. JNK1 -/- mice had decreased Influenza A burden in viral pneumonia, yet displayed worsened morbidity. Finally, JNK1 was required for IL-17A mediated induction of inflammatory cytokines and antimicrobial peptides both in epithelial cells and the lung. These data identify JNK1 as an important signaling molecule in host defense and demonstrate a pathogen specific role in disease. Manipulation of the JNK1 pathway may represent a novel therapeutic target in pneumonia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22514650</PMID><DateCompleted><Year>2012</Year><Month>08</Month><Day>30</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>4</Issue><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Differential requirement for c-Jun N-terminal kinase 1 in lung inflammation and host defense.</ArticleTitle><Pagination><MedlinePgn>e34638</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0034638</ELocationID><Abstract><AbstractText>The c-Jun N-terminal kinase (JNK) - 1 pathway has been implicated in the cellular response to stress in many tissues and models. JNK1 is known to play a role in a variety of signaling cascades, including those involved in lung disease pathogenesis. Recently, a role for JNK1 signaling in immune cell function has emerged. The goal of the present study was to determine the role of JNK1 in host defense against both bacterial and viral pneumonia, as well as the impact of JNK1 signaling on IL-17 mediated immunity. Wild type (WT) and JNK1 -/- mice were challenged with Escherichia coli, Staphylococcus aureus, or Influenza A. In addition, WT and JNK1 -/- mice and epithelial cells were stimulated with IL-17A. The impact of JNK1 deletion on pathogen clearance, inflammation, and histopathology was assessed. JNK1 was required for clearance of E. coli, inflammatory cell recruitment, and cytokine production. Interestingly, JNK1 deletion had only a small impact on the host response to S. aureus. JNK1 -/- mice had decreased Influenza A burden in viral pneumonia, yet displayed worsened morbidity. Finally, JNK1 was required for IL-17A mediated induction of inflammatory cytokines and antimicrobial peptides both in epithelial cells and the lung. These data identify JNK1 as an important signaling molecule in host defense and demonstrate a pathogen specific role in disease. Manipulation of the JNK1 pathway may represent a novel therapeutic target in pneumonia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Van der Velden</LastName><ForeName>Jos</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Vermont, Burlington, Vermont, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Janssen-Heininger</LastName><ForeName>Yvonne M W</ForeName><Initials>YM</Initials></Author><Author ValidYN="Y"><LastName>Mandalapu</LastName><ForeName>Sivanarayna</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Scheller</LastName><ForeName>Erich V</ForeName><Initials>EV</Initials></Author><Author ValidYN="Y"><LastName>Kolls</LastName><ForeName>Jay K</ForeName><Initials>JK</Initials></Author><Author ValidYN="Y"><LastName>Alcorn</LastName><ForeName>John F</ForeName><Initials>JF</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL085464</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 HL079142</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>04</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020381">Interleukin-17</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048055">Mitogen-Activated Protein Kinase 8</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020381" MajorTopicYN="N">Interleukin-17</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D048055" MajorTopicYN="N">Mitogen-Activated Protein Kinase 8</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011014" MajorTopicYN="N">Pneumonia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013211" MajorTopicYN="N">Staphylococcus aureus</DescriptorName><QualifierName 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IdType="pmc">PMC3326034</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>J Immunol. 2000 Mar 15;164(6):3222-8</Citation><ArticleIdList><ArticleId IdType="pubmed">10706714</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 2000 Apr 3;191(7):1233-40</Citation><ArticleIdList><ArticleId IdType="pubmed">10748240</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Signal. 2001 Feb;13(2):85-94</Citation><ArticleIdList><ArticleId IdType="pubmed">11257452</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2001 Apr 6;276(14):10990-8</Citation><ArticleIdList><ArticleId IdType="pubmed">11150300</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 2001 Aug 20;194(4):519-27</Citation><ArticleIdList><ArticleId IdType="pubmed">11514607</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 2001 Sep;25(3):335-40</Citation><ArticleIdList><ArticleId IdType="pubmed">11588011</ArticleId></ArticleIdList></Reference><Reference><Citation>Cytokine. 2007 Jun;38(3):157-64</Citation><ArticleIdList><ArticleId IdType="pubmed">17644350</ArticleId></ArticleIdList></Reference><Reference><Citation>J Gastroenterol. 2007 Sep;42(9):746-53</Citation><ArticleIdList><ArticleId IdType="pubmed">17876544</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Immunol. 2008 Mar;45(6):1665-73</Citation><ArticleIdList><ArticleId IdType="pubmed">17997161</ArticleId></ArticleIdList></Reference><Reference><Citation>Respirology. 2008 Mar;13(2):203-14</Citation><ArticleIdList><ArticleId IdType="pubmed">18339017</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Sci. 2008 Apr 1;121(Pt 7):1036-45</Citation><ArticleIdList><ArticleId IdType="pubmed">18334556</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2008 Nov 15;181(10):7147-56</Citation><ArticleIdList><ArticleId IdType="pubmed">18981136</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunol Rev. 2009 Mar;228(1):212-24</Citation><ArticleIdList><ArticleId IdType="pubmed">19290930</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 2009 Apr;40(4):422-32</Citation><ArticleIdList><ArticleId IdType="pubmed">18836136</ArticleId></ArticleIdList></Reference><Reference><Citation>Pulm Pharmacol Ther. 2009 Jun;22(3):199-207</Citation><ArticleIdList><ArticleId IdType="pubmed">19121406</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2009 Sep 4;284(36):24006-16</Citation><ArticleIdList><ArticleId IdType="pubmed">19592489</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2009 Oct 15;183(8):5301-10</Citation><ArticleIdList><ArticleId IdType="pubmed">19783685</ArticleId></ArticleIdList></Reference><Reference><Citation>Virology. 2010 Jan 20;396(2):178-88</Citation><ArticleIdList><ArticleId IdType="pubmed">19913271</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2010 Feb 15;184(4):2065-75</Citation><ArticleIdList><ArticleId IdType="pubmed">20083670</ArticleId></ArticleIdList></Reference><Reference><Citation>Virology. 2010 May 10;400(2):224-32</Citation><ArticleIdList><ArticleId IdType="pubmed">20185156</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2010 Apr 15;184(8):4479-87</Citation><ArticleIdList><ArticleId IdType="pubmed">20228199</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2010 May 1;184(9):4898-906</Citation><ArticleIdList><ArticleId IdType="pubmed">20351184</ArticleId></ArticleIdList></Reference><Reference><Citation>J Gen Virol. 2010 Jun;91(Pt 6):1439-49</Citation><ArticleIdList><ArticleId IdType="pubmed">20130137</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2011 Feb 1;186(3):1666-74</Citation><ArticleIdList><ArticleId IdType="pubmed">21178015</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Respir Cell Mol Biol. 2011 Apr;44(4):571-81</Citation><ArticleIdList><ArticleId IdType="pubmed">20581097</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2011 Jul;79(7):2567-77</Citation><ArticleIdList><ArticleId IdType="pubmed">21518788</ArticleId></ArticleIdList></Reference><Reference><Citation>Adv Exp Med Biol. 2012;946:237-51</Citation><ArticleIdList><ArticleId IdType="pubmed">21948372</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2011 Nov;79(11):4588-99</Citation><ArticleIdList><ArticleId IdType="pubmed">21844230</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Microbiol Rev. 2005 Jul;18(3):521-40</Citation><ArticleIdList><ArticleId IdType="pubmed">16020688</ArticleId></ArticleIdList></Reference><Reference><Citation>J Allergy Clin Immunol. 2001 Nov;108(5):804-9</Citation><ArticleIdList><ArticleId IdType="pubmed">11692108</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Immunol. 2002;20:55-72</Citation><ArticleIdList><ArticleId IdType="pubmed">11861597</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 2002 Apr 1;195(7):811-23</Citation><ArticleIdList><ArticleId IdType="pubmed">11927626</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2002 May 3;277(18):15229-32</Citation><ArticleIdList><ArticleId IdType="pubmed">11891214</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2002 Nov;76(21):11166-71</Citation><ArticleIdList><ArticleId IdType="pubmed">12368362</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunol Rev. 2003 Apr;192:131-42</Citation><ArticleIdList><ArticleId IdType="pubmed">12670401</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2004 Jan 23;279(4):2712-8</Citation><ArticleIdList><ArticleId IdType="pubmed">14600154</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1998 Dec 11;282(5396):2092-5</Citation><ArticleIdList><ArticleId IdType="pubmed">9851932</ArticleId></ArticleIdList></Reference><Reference><Citation>J Am Soc Nephrol. 2005 Jun;16(6):1603-11</Citation><ArticleIdList><ArticleId IdType="pubmed">15843470</ArticleId></ArticleIdList></Reference><Reference><Citation>J Heart Lung Transplant. 2005 Jul;24(7):875-81</Citation><ArticleIdList><ArticleId IdType="pubmed">15982617</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2006 Jul;74(7):4104-13</Citation><ArticleIdList><ArticleId IdType="pubmed">16790784</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2006 Aug 25;281(34):24138-48</Citation><ArticleIdList><ArticleId IdType="pubmed">16798734</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2006 Sep 15;177(6):4064-71</Citation><ArticleIdList><ArticleId IdType="pubmed">16951370</ArticleId></ArticleIdList></Reference><Reference><Citation>Infect Immun. 2006 Dec;74(12):6557-70</Citation><ArticleIdList><ArticleId IdType="pubmed">16966406</ArticleId></ArticleIdList></Reference><Reference><Citation>J Leukoc Biol. 2007 Feb;81(2):539-47</Citation><ArticleIdList><ArticleId IdType="pubmed">17062604</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2007 Mar 1;178(5):3153-60</Citation><ArticleIdList><ArticleId IdType="pubmed">17312163</ArticleId></ArticleIdList></Reference><Reference><Citation>Curr Opin Cell Biol. 2007 Apr;19(2):142-9</Citation><ArticleIdList><ArticleId IdType="pubmed">17303404</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol Lung Cell Mol Physiol. 2007 Jun;292(6):L1495-505</Citation><ArticleIdList><ArticleId IdType="pubmed">17307812</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol Lung Cell Mol Physiol. 2007 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