Human-origin Lactobacillus salivarius AR809 protects against immunosuppression in S. aureus-induced pharyngitis via Akt-mediated NF-κB and autophagy signaling pathways.
Identifieur interne : 000112 ( Main/Exploration ); précédent : 000111; suivant : 000113Human-origin Lactobacillus salivarius AR809 protects against immunosuppression in S. aureus-induced pharyngitis via Akt-mediated NF-κB and autophagy signaling pathways.
Auteurs : Guochao Jia [République populaire de Chine] ; Xiaofeng Liu ; Na Che ; Yongjun Xia ; Guangqiang Wang ; Zhiqiang Xiong ; Hui Zhang ; Lianzhong AiSource :
- Food & function [ 2042-650X ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Autophagie (MeSH), Cyclooxygenase 2 (métabolisme), Cytokines (métabolisme), Dinoprostone (métabolisme), Facteur de nécrose tumorale alpha (métabolisme), Facteur de transcription RelA (métabolisme), Inflammation (métabolisme), Lactobacillus salivarius (MeSH), Macrophages (cytologie), Monoxyde d'azote (métabolisme), Mâle (MeSH), Pharyngite (microbiologie), Pharyngite (thérapie), Phosphatidylinositol 3-kinases (métabolisme), Probiotiques (MeSH), Protéines proto-oncogènes c-akt (métabolisme), Souris (MeSH), Souris de lignée ICR (MeSH), Staphylococcus aureus (pathogénicité), Transduction du signal (MeSH).
- MESH :
- cytologie : Macrophages.
- microbiologie : Pharyngite.
- métabolisme : Cyclooxygenase 2, Cytokines, Dinoprostone, Facteur de nécrose tumorale alpha, Facteur de transcription RelA, Inflammation, Monoxyde d'azote, Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- pathogénicité : Staphylococcus aureus.
- thérapie : Pharyngite.
- Animaux, Autophagie, Lactobacillus salivarius, Mâle, Probiotiques, Souris, Souris de lignée ICR, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Autophagy (MeSH), Cyclooxygenase 2 (metabolism), Cytokines (metabolism), Dinoprostone (metabolism), Inflammation (metabolism), Lactobacillus salivarius (MeSH), Macrophages (cytology), Male (MeSH), Mice (MeSH), Mice, Inbred ICR (MeSH), Nitric Oxide (metabolism), Pharyngitis (microbiology), Pharyngitis (therapy), Phosphatidylinositol 3-Kinases (metabolism), Probiotics (MeSH), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (MeSH), Staphylococcus aureus (pathogenicity), Transcription Factor RelA (metabolism), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , metabolism : Cyclooxygenase 2, Cytokines, Dinoprostone, Nitric Oxide, Proto-Oncogene Proteins c-akt, Transcription Factor RelA, Tumor Necrosis Factor-alpha.
- cytology : Macrophages.
- metabolism : Inflammation, Phosphatidylinositol 3-Kinases.
- microbiology : Pharyngitis.
- pathogenicity : Staphylococcus aureus.
- therapy : Pharyngitis.
- Animals, Autophagy, Lactobacillus salivarius, Male, Mice, Mice, Inbred ICR, Probiotics, Signal Transduction.
Abstract
Lactobacillus salivarius AR809 is a newly discovered probiotic strain from a healthy human pharynx and has potential ability to adhere to the pharyngeal epithelium and inhibit Staphylococcus aureus (S. aureus)-induced inflammatory response. Pharyngeal spray administration of AR809 exhibited protective effects in a S. aureus-induced mouse model of pharyngitis. The inhibitory effect and underlying molecular mechanism of AR809 on S. aureus-stimulated pharyngitis were further investigated. AR809 significantly increased phagocytosis and bactericidal activity, reduced the production of inflammatory mediators (intracellular reactive oxygen species (ROS), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nitric oxide (NO), inducible NOS (iNOS)) and the expression of inflammatory cytokines (tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)), and induced macrophages to adopt the M2 phenotype. AR809 also attenuated S. aureus-induced phosphorylations of protein kinase B (Akt) and rapamycin (mTOR), and elevated the autophagic protein (light chain 3 from II (LC3-II) and Beclin-1) level. Furthermore, AR809 inhibited nuclear transcription factor kappa-B (NF-κB) activation by suppressing the nuclear translocation of NF-κB p65. Likewise, 740Y-P (a PI3K activator) decreased the anti-inflammatory effect of AR809 against S. aureus-induced inflammatory response, while AR809 treatments with wortmannin (a PI3K inhibitor) markedly reversed this inflammatory response. AR809 prevents S. aureus-induced pharyngeal inflammatory response, possibly by regulating TLR/PI3K/Akt/mTOR signalling pathway-related autophagy and TLR/PI3K/Akt/IκB/NF-κB pathway activity, and therefore has potential for use in preventing pharyngitis and other inflammatory diseases.
DOI: 10.1039/c9fo02476j
PubMed: 31957758
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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sortKey="Liu, Xiaofeng" sort="Liu, Xiaofeng" uniqKey="Liu X" first="Xiaofeng" last="Liu">Xiaofeng Liu</name></author><author><name sortKey="Che, Na" sort="Che, Na" uniqKey="Che N" first="Na" last="Che">Na Che</name></author><author><name sortKey="Xia, Yongjun" sort="Xia, Yongjun" uniqKey="Xia Y" first="Yongjun" last="Xia">Yongjun Xia</name></author><author><name sortKey="Wang, Guangqiang" sort="Wang, Guangqiang" uniqKey="Wang G" first="Guangqiang" last="Wang">Guangqiang Wang</name></author><author><name sortKey="Xiong, Zhiqiang" sort="Xiong, Zhiqiang" uniqKey="Xiong Z" first="Zhiqiang" last="Xiong">Zhiqiang Xiong</name></author><author><name sortKey="Zhang, Hui" sort="Zhang, Hui" uniqKey="Zhang H" first="Hui" last="Zhang">Hui Zhang</name></author><author><name sortKey="Ai, Lianzhong" sort="Ai, Lianzhong" uniqKey="Ai L" first="Lianzhong" last="Ai">Lianzhong Ai</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno 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Science and Technology, Shanghai 200093, China. ailianzhong1@126.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai Engineering Research Center of Food Microbiology, School of Medical Instrument and Food Engineering, University of Shanghai for Science and Technology, Shanghai 200093</wicri:regionArea><wicri:noRegion>Shanghai 200093</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Xiaofeng" sort="Liu, Xiaofeng" uniqKey="Liu X" first="Xiaofeng" last="Liu">Xiaofeng Liu</name></author><author><name sortKey="Che, Na" sort="Che, Na" uniqKey="Che N" first="Na" last="Che">Na Che</name></author><author><name sortKey="Xia, Yongjun" sort="Xia, Yongjun" uniqKey="Xia Y" first="Yongjun" last="Xia">Yongjun Xia</name></author><author><name sortKey="Wang, Guangqiang" sort="Wang, Guangqiang" uniqKey="Wang G" first="Guangqiang" last="Wang">Guangqiang Wang</name></author><author><name sortKey="Xiong, Zhiqiang" sort="Xiong, Zhiqiang" uniqKey="Xiong Z" first="Zhiqiang" last="Xiong">Zhiqiang Xiong</name></author><author><name sortKey="Zhang, Hui" sort="Zhang, Hui" uniqKey="Zhang H" first="Hui" last="Zhang">Hui Zhang</name></author><author><name sortKey="Ai, Lianzhong" sort="Ai, Lianzhong" uniqKey="Ai L" first="Lianzhong" last="Ai">Lianzhong Ai</name></author></analytic><series><title level="j">Food & function</title><idno type="eISSN">2042-650X</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Autophagy (MeSH)</term><term>Cyclooxygenase 2 (metabolism)</term><term>Cytokines (metabolism)</term><term>Dinoprostone (metabolism)</term><term>Inflammation (metabolism)</term><term>Lactobacillus salivarius (MeSH)</term><term>Macrophages (cytology)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Inbred ICR (MeSH)</term><term>Nitric Oxide (metabolism)</term><term>Pharyngitis (microbiology)</term><term>Pharyngitis (therapy)</term><term>Phosphatidylinositol 3-Kinases (metabolism)</term><term>Probiotics (MeSH)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Staphylococcus aureus (pathogenicity)</term><term>Transcription Factor RelA (metabolism)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Autophagie (MeSH)</term><term>Cyclooxygenase 2 (métabolisme)</term><term>Cytokines (métabolisme)</term><term>Dinoprostone (métabolisme)</term><term>Facteur de nécrose tumorale alpha (métabolisme)</term><term>Facteur de transcription RelA (métabolisme)</term><term>Inflammation (métabolisme)</term><term>Lactobacillus salivarius (MeSH)</term><term>Macrophages (cytologie)</term><term>Monoxyde d'azote (métabolisme)</term><term>Mâle (MeSH)</term><term>Pharyngite (microbiologie)</term><term>Pharyngite (thérapie)</term><term>Phosphatidylinositol 3-kinases (métabolisme)</term><term>Probiotiques (MeSH)</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Souris (MeSH)</term><term>Souris de lignée ICR (MeSH)</term><term>Staphylococcus aureus (pathogénicité)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclooxygenase 2</term><term>Cytokines</term><term>Dinoprostone</term><term>Nitric Oxide</term><term>Proto-Oncogene Proteins c-akt</term><term>Transcription Factor RelA</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inflammation</term><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Pharyngite</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Pharyngitis</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cyclooxygenase 2</term><term>Cytokines</term><term>Dinoprostone</term><term>Facteur de nécrose tumorale alpha</term><term>Facteur de transcription RelA</term><term>Inflammation</term><term>Monoxyde d'azote</term><term>Phosphatidylinositol 3-kinases</term><term>Protéines proto-oncogènes c-akt</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Staphylococcus aureus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Staphylococcus aureus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Pharyngitis</term></keywords><keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Pharyngite</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autophagy</term><term>Lactobacillus salivarius</term><term>Male</term><term>Mice</term><term>Mice, Inbred ICR</term><term>Probiotics</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Autophagie</term><term>Lactobacillus salivarius</term><term>Mâle</term><term>Probiotiques</term><term>Souris</term><term>Souris de lignée ICR</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lactobacillus salivarius AR809 is a newly discovered probiotic strain from a healthy human pharynx and has potential ability to adhere to the pharyngeal epithelium and inhibit Staphylococcus aureus (S. aureus)-induced inflammatory response. Pharyngeal spray administration of AR809 exhibited protective effects in a S. aureus-induced mouse model of pharyngitis. The inhibitory effect and underlying molecular mechanism of AR809 on S. aureus-stimulated pharyngitis were further investigated. AR809 significantly increased phagocytosis and bactericidal activity, reduced the production of inflammatory mediators (intracellular reactive oxygen species (ROS), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nitric oxide (NO), inducible NOS (iNOS)) and the expression of inflammatory cytokines (tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)), and induced macrophages to adopt the M2 phenotype. AR809 also attenuated S. aureus-induced phosphorylations of protein kinase B (Akt) and rapamycin (mTOR), and elevated the autophagic protein (light chain 3 from II (LC3-II) and Beclin-1) level. Furthermore, AR809 inhibited nuclear transcription factor kappa-B (NF-κB) activation by suppressing the nuclear translocation of NF-κB p65. Likewise, 740Y-P (a PI3K activator) decreased the anti-inflammatory effect of AR809 against S. aureus-induced inflammatory response, while AR809 treatments with wortmannin (a PI3K inhibitor) markedly reversed this inflammatory response. AR809 prevents S. aureus-induced pharyngeal inflammatory response, possibly by regulating TLR/PI3K/Akt/mTOR signalling pathway-related autophagy and TLR/PI3K/Akt/IκB/NF-κB pathway activity, and therefore has potential for use in preventing pharyngitis and other inflammatory diseases.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31957758</PMID><DateCompleted><Year>2020</Year><Month>10</Month><Day>07</Day></DateCompleted><DateRevised><Year>2020</Year><Month>10</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2042-650X</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>Jan</Month><Day>29</Day></PubDate></JournalIssue><Title>Food & function</Title><ISOAbbreviation>Food Funct</ISOAbbreviation></Journal><ArticleTitle>Human-origin Lactobacillus salivarius AR809 protects against immunosuppression in S. aureus-induced pharyngitis via Akt-mediated NF-κB and autophagy signaling pathways.</ArticleTitle><Pagination><MedlinePgn>270-284</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1039/c9fo02476j</ELocationID><Abstract><AbstractText>Lactobacillus salivarius AR809 is a newly discovered probiotic strain from a healthy human pharynx and has potential ability to adhere to the pharyngeal epithelium and inhibit Staphylococcus aureus (S. aureus)-induced inflammatory response. Pharyngeal spray administration of AR809 exhibited protective effects in a S. aureus-induced mouse model of pharyngitis. The inhibitory effect and underlying molecular mechanism of AR809 on S. aureus-stimulated pharyngitis were further investigated. AR809 significantly increased phagocytosis and bactericidal activity, reduced the production of inflammatory mediators (intracellular reactive oxygen species (ROS), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nitric oxide (NO), inducible NOS (iNOS)) and the expression of inflammatory cytokines (tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)), and induced macrophages to adopt the M2 phenotype. AR809 also attenuated S. aureus-induced phosphorylations of protein kinase B (Akt) and rapamycin (mTOR), and elevated the autophagic protein (light chain 3 from II (LC3-II) and Beclin-1) level. Furthermore, AR809 inhibited nuclear transcription factor kappa-B (NF-κB) activation by suppressing the nuclear translocation of NF-κB p65. Likewise, 740Y-P (a PI3K activator) decreased the anti-inflammatory effect of AR809 against S. aureus-induced inflammatory response, while AR809 treatments with wortmannin (a PI3K inhibitor) markedly reversed this inflammatory response. AR809 prevents S. aureus-induced pharyngeal inflammatory response, possibly by regulating TLR/PI3K/Akt/mTOR signalling pathway-related autophagy and TLR/PI3K/Akt/IκB/NF-κB pathway activity, and therefore has potential for use in preventing pharyngitis and other inflammatory diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jia</LastName><ForeName>Guochao</ForeName><Initials>G</Initials><Suffix></Suffix><AffiliationInfo><Affiliation>Shanghai Engineering Research Center of Food Microbiology, School of Medical Instrument and Food Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China. ailianzhong1@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xiaofeng</ForeName><Initials>X</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Che</LastName><ForeName>Na</ForeName><Initials>N</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Xia</LastName><ForeName>Yongjun</ForeName><Initials>Y</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Guangqiang</ForeName><Initials>G</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Xiong</LastName><ForeName>Zhiqiang</ForeName><Initials>Z</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Hui</ForeName><Initials>H</Initials><Suffix></Suffix></Author><Author ValidYN="Y"><LastName>Ai</LastName><ForeName>Lianzhong</ForeName><Initials>L</Initials><Suffix></Suffix></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Food Funct</MedlineTA><NlmUniqueID>101549033</NlmUniqueID><ISSNLinking>2042-6496</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C498144">Rela protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051996">Transcription Factor RelA</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.99.-</RegistryNumber><NameOfSubstance UI="C077623">Ptgs2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.99.1</RegistryNumber><NameOfSubstance UI="D051546">Cyclooxygenase 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>K7Q1JQR04M</RegistryNumber><NameOfSubstance UI="D015232">Dinoprostone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051546" MajorTopicYN="N">Cyclooxygenase 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015232" MajorTopicYN="N">Dinoprostone</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069996" MajorTopicYN="Y">Lactobacillus salivarius</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008813" MajorTopicYN="N">Mice, Inbred ICR</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010612" MajorTopicYN="N">Pharyngitis</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019936" MajorTopicYN="N">Probiotics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="Y">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013211" MajorTopicYN="N">Staphylococcus aureus</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051996" MajorTopicYN="N">Transcription Factor RelA</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>1</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31957758</ArticleId><ArticleId IdType="doi">10.1039/c9fo02476j</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Ai, Lianzhong" sort="Ai, Lianzhong" uniqKey="Ai L" first="Lianzhong" last="Ai">Lianzhong Ai</name><name sortKey="Che, Na" sort="Che, Na" uniqKey="Che N" first="Na" last="Che">Na Che</name><name sortKey="Liu, Xiaofeng" sort="Liu, Xiaofeng" uniqKey="Liu X" first="Xiaofeng" last="Liu">Xiaofeng Liu</name><name sortKey="Wang, Guangqiang" sort="Wang, Guangqiang" uniqKey="Wang G" first="Guangqiang" last="Wang">Guangqiang Wang</name><name sortKey="Xia, Yongjun" sort="Xia, Yongjun" uniqKey="Xia Y" first="Yongjun" last="Xia">Yongjun Xia</name><name sortKey="Xiong, Zhiqiang" sort="Xiong, Zhiqiang" uniqKey="Xiong Z" first="Zhiqiang" last="Xiong">Zhiqiang Xiong</name><name sortKey="Zhang, Hui" sort="Zhang, Hui" uniqKey="Zhang H" first="Hui" last="Zhang">Hui Zhang</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Jia, Guochao" sort="Jia, Guochao" uniqKey="Jia G" first="Guochao" last="Jia">Guochao 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