Intratracheal administration of mitochondrial DNA directly provokes lung inflammation through the TLR9-p38 MAPK pathway.
Identifieur interne : 000265 ( PubMed/Curation ); précédent : 000264; suivant : 000266Intratracheal administration of mitochondrial DNA directly provokes lung inflammation through the TLR9-p38 MAPK pathway.
Auteurs : Xiaoling Gu [République populaire de Chine] ; Guannan Wu [République populaire de Chine] ; Yanwen Yao [République populaire de Chine] ; Junli Zeng [République populaire de Chine] ; Donghong Shi [République populaire de Chine] ; Tangfeng Lv [République populaire de Chine] ; Liang Luo [République populaire de Chine] ; Yong Song [République populaire de Chine]Source :
- Free radical biology & medicine [ 1873-4596 ] ; 2015.
Descripteurs français
- KwdFr :
- ADN mitochondrial (administration et posologie), ADN mitochondrial (métabolisme), Animaux, Cytokines, Macrophages (anatomopathologie), Macrophages (métabolisme), Mâle, Phosphorylation, Pneumopathie infectieuse (anatomopathologie), Pneumopathie infectieuse (génétique), Pneumopathie infectieuse (métabolisme), Récepteur-9 de type Toll-like (métabolisme), Souris, Souris de lignée C57BL, Technique d'immunofluorescence, Technique de Western, Test ELISA, Trachée, Transduction du signal, Voies d'administration de substances chimiques et des médicaments, p38 Mitogen-Activated Protein Kinases (métabolisme).
- MESH :
- administration et posologie : ADN mitochondrial.
- anatomopathologie : Macrophages, Pneumopathie infectieuse.
- génétique : Pneumopathie infectieuse.
- métabolisme : ADN mitochondrial, Macrophages, Pneumopathie infectieuse, Récepteur-9 de type Toll-like, p38 Mitogen-Activated Protein Kinases.
- Animaux, Cytokines, Mâle, Phosphorylation, Souris, Souris de lignée C57BL, Technique d'immunofluorescence, Technique de Western, Test ELISA, Trachée, Transduction du signal, Voies d'administration de substances chimiques et des médicaments.
English descriptors
- KwdEn :
- Animals, Blotting, Western, Cytokines, DNA, Mitochondrial (administration & dosage), DNA, Mitochondrial (metabolism), Drug Administration Routes, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Macrophages (metabolism), Macrophages (pathology), Male, Mice, Mice, Inbred C57BL, Phosphorylation, Pneumonia (genetics), Pneumonia (metabolism), Pneumonia (pathology), Signal Transduction, Toll-Like Receptor 9 (metabolism), Trachea, p38 Mitogen-Activated Protein Kinases (metabolism).
- MESH :
- chemical , administration & dosage : DNA, Mitochondrial.
- chemical , metabolism : DNA, Mitochondrial, Toll-Like Receptor 9, p38 Mitogen-Activated Protein Kinases.
- chemical : Cytokines.
- genetics : Pneumonia.
- metabolism : Macrophages, Pneumonia.
- pathology : Macrophages, Pneumonia.
- Animals, Blotting, Western, Drug Administration Routes, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Male, Mice, Mice, Inbred C57BL, Phosphorylation, Signal Transduction, Trachea.
Abstract
An increasing number of studies have focused on the phenomenon that mitochondrial DNA (mtDNA) activates innate immunity responses. However, the specific role of mtDNA in inflammatory lung disease remains elusive. This study was designed to examine the proinflammatory effects of mtDNA in lungs and to investigate the putative mechanisms. C57BL/6 mice were challenged intratracheally with mtDNA with or without pretreatment with chloroquine. Changes in pulmonary histopathology, cytokine concentrations, and phosphorylation levels of p38 MAPK were assayed at four time points. In in vitro experiments, THP-1 macrophages were pretreated or not pretreated with chloroquine, TLR9 siRNA, p38 MAPK siRNA, or SB203580 and then incubated with mtDNA. The levels of cytokines and p-p38 MAPK were detected by ELISA and Western blot, respectively. The intratracheal administration of mtDNA induced infiltration of inflammatory cells, production of proinflammatory cytokines (including IL-1β, IL-6, and TNF-α), and activation of p38 MAPK. The chloroquine pretreatment resulted in an abatement of mtDNA-induced local lung inflammation. In vitro experiments showed that the exposure of THP-1 macrophages to mtDNA also led to a significant upregulation of IL-1β, IL-6, and TNF-α and the activation of p38 MAPK. And these responses were inhibited either by chloroquine and TLR9 siRNA or by SB203580 and p38 MAPK siRNA pretreatment. The intratracheal administration of mtDNA induced a local inflammatory response in the mouse lung that depended on the interactions of mtDNA with TLR9 and may be correlated with infiltrating macrophages that could be activated by mtDNA exposure via the TLR9-p38 MAPK signal transduction pathway.
DOI: 10.1016/j.freeradbiomed.2015.02.034
PubMed: 25772007
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Electronic address: yong_song6310@yahoo.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25772007</idno><idno type="pmid">25772007</idno><idno type="doi">10.1016/j.freeradbiomed.2015.02.034</idno><idno type="wicri:Area/PubMed/Corpus">000265</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000265</idno><idno type="wicri:Area/PubMed/Curation">000265</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000265</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Intratracheal administration of mitochondrial DNA directly provokes lung inflammation through the TLR9-p38 MAPK pathway.</title><author><name sortKey="Gu, Xiaoling" sort="Gu, Xiaoling" uniqKey="Gu X" first="Xiaoling" last="Gu">Xiaoling Gu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author><author><name sortKey="Wu, Guannan" sort="Wu, Guannan" uniqKey="Wu G" first="Guannan" last="Wu">Guannan Wu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author><author><name sortKey="Yao, Yanwen" sort="Yao, Yanwen" uniqKey="Yao Y" first="Yanwen" last="Yao">Yanwen Yao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author><author><name sortKey="Zeng, Junli" sort="Zeng, Junli" uniqKey="Zeng J" first="Junli" last="Zeng">Junli Zeng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author><author><name sortKey="Shi, Donghong" sort="Shi, Donghong" uniqKey="Shi D" first="Donghong" last="Shi">Donghong Shi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Imaging, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Medical Imaging, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author><author><name sortKey="Lv, Tangfeng" sort="Lv, Tangfeng" uniqKey="Lv T" first="Tangfeng" last="Lv">Tangfeng Lv</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author><author><name sortKey="Luo, Liang" sort="Luo, Liang" uniqKey="Luo L" first="Liang" last="Luo">Liang Luo</name><affiliation wicri:level="1"><nlm:affiliation>Intensive Care Unit, Wuxi Second Affiliated Hospital, Nanjing Medical University, Wuxi, Jiangsu Province 210004, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Intensive Care Unit, Wuxi Second Affiliated Hospital, Nanjing Medical University, Wuxi, Jiangsu Province 210004</wicri:regionArea></affiliation></author><author><name sortKey="Song, Yong" sort="Song, Yong" uniqKey="Song Y" first="Yong" last="Song">Yong Song</name><affiliation wicri:level="1"><nlm:affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China. Electronic address: yong_song6310@yahoo.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002</wicri:regionArea></affiliation></author></analytic><series><title level="j">Free radical biology & medicine</title><idno type="eISSN">1873-4596</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Cytokines</term><term>DNA, Mitochondrial (administration & dosage)</term><term>DNA, Mitochondrial (metabolism)</term><term>Drug Administration Routes</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Fluorescent Antibody Technique</term><term>Macrophages (metabolism)</term><term>Macrophages (pathology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Phosphorylation</term><term>Pneumonia (genetics)</term><term>Pneumonia (metabolism)</term><term>Pneumonia (pathology)</term><term>Signal Transduction</term><term>Toll-Like Receptor 9 (metabolism)</term><term>Trachea</term><term>p38 Mitogen-Activated Protein Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN mitochondrial (administration et posologie)</term><term>ADN mitochondrial (métabolisme)</term><term>Animaux</term><term>Cytokines</term><term>Macrophages (anatomopathologie)</term><term>Macrophages (métabolisme)</term><term>Mâle</term><term>Phosphorylation</term><term>Pneumopathie infectieuse (anatomopathologie)</term><term>Pneumopathie infectieuse (génétique)</term><term>Pneumopathie infectieuse (métabolisme)</term><term>Récepteur-9 de type Toll-like (métabolisme)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Technique d'immunofluorescence</term><term>Technique de Western</term><term>Test ELISA</term><term>Trachée</term><term>Transduction du signal</term><term>Voies d'administration de substances chimiques et des médicaments</term><term>p38 Mitogen-Activated Protein Kinases (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>DNA, Mitochondrial</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>DNA, Mitochondrial</term><term>Toll-Like Receptor 9</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>ADN mitochondrial</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Macrophages</term><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</term><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ADN mitochondrial</term><term>Macrophages</term><term>Pneumopathie infectieuse</term><term>Récepteur-9 de type Toll-like</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Macrophages</term><term>Pneumonia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Blotting, Western</term><term>Drug Administration Routes</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Fluorescent Antibody Technique</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Phosphorylation</term><term>Signal Transduction</term><term>Trachea</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cytokines</term><term>Mâle</term><term>Phosphorylation</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Technique d'immunofluorescence</term><term>Technique de Western</term><term>Test ELISA</term><term>Trachée</term><term>Transduction du signal</term><term>Voies d'administration de substances chimiques et des médicaments</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">An increasing number of studies have focused on the phenomenon that mitochondrial DNA (mtDNA) activates innate immunity responses. However, the specific role of mtDNA in inflammatory lung disease remains elusive. This study was designed to examine the proinflammatory effects of mtDNA in lungs and to investigate the putative mechanisms. C57BL/6 mice were challenged intratracheally with mtDNA with or without pretreatment with chloroquine. Changes in pulmonary histopathology, cytokine concentrations, and phosphorylation levels of p38 MAPK were assayed at four time points. In in vitro experiments, THP-1 macrophages were pretreated or not pretreated with chloroquine, TLR9 siRNA, p38 MAPK siRNA, or SB203580 and then incubated with mtDNA. The levels of cytokines and p-p38 MAPK were detected by ELISA and Western blot, respectively. The intratracheal administration of mtDNA induced infiltration of inflammatory cells, production of proinflammatory cytokines (including IL-1β, IL-6, and TNF-α), and activation of p38 MAPK. The chloroquine pretreatment resulted in an abatement of mtDNA-induced local lung inflammation. In vitro experiments showed that the exposure of THP-1 macrophages to mtDNA also led to a significant upregulation of IL-1β, IL-6, and TNF-α and the activation of p38 MAPK. And these responses were inhibited either by chloroquine and TLR9 siRNA or by SB203580 and p38 MAPK siRNA pretreatment. The intratracheal administration of mtDNA induced a local inflammatory response in the mouse lung that depended on the interactions of mtDNA with TLR9 and may be correlated with infiltrating macrophages that could be activated by mtDNA exposure via the TLR9-p38 MAPK signal transduction pathway. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25772007</PMID><DateCompleted><Year>2016</Year><Month>03</Month><Day>14</Day></DateCompleted><DateRevised><Year>2015</Year><Month>05</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-4596</ISSN><JournalIssue CitedMedium="Internet"><Volume>83</Volume><PubDate><Year>2015</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Free radical biology & medicine</Title><ISOAbbreviation>Free Radic. Biol. Med.</ISOAbbreviation></Journal><ArticleTitle>Intratracheal administration of mitochondrial DNA directly provokes lung inflammation through the TLR9-p38 MAPK pathway.</ArticleTitle><Pagination><MedlinePgn>149-58</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.freeradbiomed.2015.02.034</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0891-5849(15)00111-2</ELocationID><Abstract><AbstractText>An increasing number of studies have focused on the phenomenon that mitochondrial DNA (mtDNA) activates innate immunity responses. However, the specific role of mtDNA in inflammatory lung disease remains elusive. This study was designed to examine the proinflammatory effects of mtDNA in lungs and to investigate the putative mechanisms. C57BL/6 mice were challenged intratracheally with mtDNA with or without pretreatment with chloroquine. Changes in pulmonary histopathology, cytokine concentrations, and phosphorylation levels of p38 MAPK were assayed at four time points. In in vitro experiments, THP-1 macrophages were pretreated or not pretreated with chloroquine, TLR9 siRNA, p38 MAPK siRNA, or SB203580 and then incubated with mtDNA. The levels of cytokines and p-p38 MAPK were detected by ELISA and Western blot, respectively. The intratracheal administration of mtDNA induced infiltration of inflammatory cells, production of proinflammatory cytokines (including IL-1β, IL-6, and TNF-α), and activation of p38 MAPK. The chloroquine pretreatment resulted in an abatement of mtDNA-induced local lung inflammation. In vitro experiments showed that the exposure of THP-1 macrophages to mtDNA also led to a significant upregulation of IL-1β, IL-6, and TNF-α and the activation of p38 MAPK. And these responses were inhibited either by chloroquine and TLR9 siRNA or by SB203580 and p38 MAPK siRNA pretreatment. The intratracheal administration of mtDNA induced a local inflammatory response in the mouse lung that depended on the interactions of mtDNA with TLR9 and may be correlated with infiltrating macrophages that could be activated by mtDNA exposure via the TLR9-p38 MAPK signal transduction pathway. </AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Xiaoling</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Guannan</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Yanwen</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zeng</LastName><ForeName>Junli</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Donghong</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Medical Imaging, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lv</LastName><ForeName>Tangfeng</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luo</LastName><ForeName>Liang</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Intensive Care Unit, Wuxi Second Affiliated Hospital, Nanjing Medical University, Wuxi, Jiangsu Province 210004, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Yong</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province 210002, People's Republic of China. Electronic address: yong_song6310@yahoo.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>03</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Free Radic Biol Med</MedlineTA><NlmUniqueID>8709159</NlmUniqueID><ISSNLinking>0891-5849</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004272">DNA, Mitochondrial</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495370">Tlr9 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051217">Toll-Like Receptor 9</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048051">p38 Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004272" MajorTopicYN="N">DNA, Mitochondrial</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004333" 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MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Lung</Keyword><Keyword MajorTopicYN="N">Mitochondrial DNA</Keyword><Keyword MajorTopicYN="N">TLR9–p38 MAPK signal transduction pathway</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>11</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>02</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>02</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>3</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>3</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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