Mycobacterium tuberculosis-Secreted Protein, ESAT-6, Inhibits Lipopolysaccharide-Induced MMP-9 Expression and Inflammation Through NF-κB and MAPK Signaling in RAW 264.7 Macrophage Cells.
Identifieur interne : 000059 ( Main/Exploration ); précédent : 000058; suivant : 000060Mycobacterium tuberculosis-Secreted Protein, ESAT-6, Inhibits Lipopolysaccharide-Induced MMP-9 Expression and Inflammation Through NF-κB and MAPK Signaling in RAW 264.7 Macrophage Cells.
Auteurs : Sun-Hyung Ha [Corée du Sud] ; Hyunju Choi [Corée du Sud] ; Jun-Young Park [Corée du Sud] ; Fukushi Abekura [Corée du Sud] ; Young-Choon Lee [Corée du Sud] ; Jeong-Ran Kim [Corée du Sud] ; Cheorl-Ho Kim [Corée du Sud]Source :
- Inflammation [ 1573-2576 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Anti-inflammatoires (pharmacologie), Antigènes bactériens (pharmacologie), Cellules RAW 264.7 (MeSH), Cyclooxygenase 2 (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Inflammation (enzymologie), Inflammation (induit chimiquement), Inflammation (prévention et contrôle), Lipopolysaccharides (toxicité), Macrophages (effets des médicaments et des substances chimiques), Macrophages (enzymologie), Matrix metalloproteinase 9 (génétique), Matrix metalloproteinase 9 (métabolisme), Mitogen-Activated Protein Kinases (métabolisme), Monoxyde d'azote (métabolisme), Mouvement cellulaire (effets des médicaments et des substances chimiques), Nitric oxide synthase type II (métabolisme), Phosphorylation (MeSH), Protéines bactériennes (pharmacologie), Souris (MeSH), Transduction du signal (MeSH).
- MESH :
- effets des médicaments et des substances chimiques : Macrophages, Mouvement cellulaire.
- enzymologie : Inflammation, Macrophages.
- génétique : Matrix metalloproteinase 9.
- induit chimiquement : Inflammation.
- métabolisme : Cyclooxygenase 2, Facteur de transcription NF-kappa B, Matrix metalloproteinase 9, Mitogen-Activated Protein Kinases, Monoxyde d'azote, Nitric oxide synthase type II.
- pharmacologie : Anti-inflammatoires, Antigènes bactériens, Protéines bactériennes.
- prévention et contrôle : Inflammation.
- toxicité : Lipopolysaccharides.
- Animaux, Cellules RAW 264.7, Phosphorylation, Souris, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Anti-Inflammatory Agents (pharmacology), Antigens, Bacterial (pharmacology), Bacterial Proteins (pharmacology), Cell Movement (drug effects), Cyclooxygenase 2 (metabolism), Inflammation (chemically induced), Inflammation (enzymology), Inflammation (prevention & control), Lipopolysaccharides (toxicity), Macrophages (drug effects), Macrophages (enzymology), Matrix Metalloproteinase 9 (genetics), Matrix Metalloproteinase 9 (metabolism), Mice (MeSH), Mitogen-Activated Protein Kinases (metabolism), NF-kappa B (metabolism), Nitric Oxide (metabolism), Nitric Oxide Synthase Type II (metabolism), Phosphorylation (MeSH), RAW 264.7 Cells (MeSH), Signal Transduction (MeSH).
- MESH :
- chemical , genetics : Matrix Metalloproteinase 9.
- chemical , metabolism : Cyclooxygenase 2, Matrix Metalloproteinase 9, Mitogen-Activated Protein Kinases, NF-kappa B, Nitric Oxide, Nitric Oxide Synthase Type II.
- chemical , pharmacology : Anti-Inflammatory Agents, Antigens, Bacterial, Bacterial Proteins.
- chemically induced : Inflammation.
- drug effects : Cell Movement, Macrophages.
- enzymology : Inflammation, Macrophages.
- prevention & control : Inflammation.
- chemical , toxicity : Lipopolysaccharides.
- Animals, Mice, Phosphorylation, RAW 264.7 Cells, Signal Transduction.
Abstract
-20pt?>Mycobacterium tuberculosis (Mtb) is a pathogenic bacterium that causes contagious tuberculosis (TB). Recently, Mtb-secreted proteins have been considered virulence factors and candidates for drugs and vaccines. Among these proteins, 6-kDa early secreted antigenic target (ESAT-6) is known to be able to induce component of matrix metalloproteinase-9 (MMP-9) in epithelial cells, leading to recruitment of macrophages. However, detailed function of ESAT-6 during macrophage recruitment to inflammatory sites remains unknown. Thus, the objective of the present study was to elucidate such function of EAST-6 and mechanism(s) involved. In the present study, we have found that recombinant ESAT-6 purified in the form of ESAT-6 double-connected structure (2E6D) could inhibit lipopolysaccharide (LPS)-induced potential of cell migration and inflammation in murine macrophage cells. Interestingly, 2E6D suppressed LPS-induced MMP-9 expression at both protein and mRNA levels as well as its enzyme activity. Levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) enzymes as known upregulators of MMP-9 were significantly decreased when 2E6D has been treated. In addition, nitric oxide (NO) as a second messenger was also significantly decreased by treatment with the purified 2E6D. Furthermore, 2E6D inhibited LPS-induced phosphorylation of IκB and translocation of NF-κB. Moreover, 2E6D suppressed phosphorylation of MAPK signaling proteins. Taken together, these results suggest that ESAT-6 can suppress LPS-induced MMP-9 and inflammation by downregulating COX-2, iNOS, and NO through NF-κB and MAPK signaling.
DOI: 10.1007/s10753-019-01087-x
PubMed: 31720987
Affiliations:
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Sud</country><wicri:regionArea>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do</wicri:regionArea><wicri:noRegion>Kyunggi-do</wicri:noRegion></affiliation></author><author><name sortKey="Choi, Hyunju" sort="Choi, Hyunju" uniqKey="Choi H" first="Hyunju" last="Choi">Hyunju Choi</name><affiliation wicri:level="1"><nlm:affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do</wicri:regionArea><wicri:noRegion>Kyunggi-do</wicri:noRegion></affiliation></author><author><name sortKey="Park, Jun Young" sort="Park, Jun Young" uniqKey="Park J" first="Jun-Young" last="Park">Jun-Young Park</name><affiliation wicri:level="1"><nlm:affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do</wicri:regionArea><wicri:noRegion>Kyunggi-do</wicri:noRegion></affiliation></author><author><name sortKey="Abekura, Fukushi" sort="Abekura, Fukushi" uniqKey="Abekura F" first="Fukushi" last="Abekura">Fukushi Abekura</name><affiliation wicri:level="1"><nlm:affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do</wicri:regionArea><wicri:noRegion>Kyunggi-do</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Young Choon" sort="Lee, Young Choon" uniqKey="Lee Y" first="Young-Choon" last="Lee">Young-Choon Lee</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Medicinal Biotechnology, Dong-A University, Busan, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Faculty of Medicinal Biotechnology, Dong-A University, Busan</wicri:regionArea><wicri:noRegion>Busan</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Jeong Ran" sort="Kim, Jeong Ran" uniqKey="Kim J" first="Jeong-Ran" last="Kim">Jeong-Ran Kim</name><affiliation wicri:level="1"><nlm:affiliation>Department of Research and Development, The Korean Institute of Tuberculosis, 168-5 Osongsaengmyeong4-ro, Heungdeok-gu, Cheongju-si, 28158, Chungcheongbuk-do, Republic of Korea. happyjrk@knta.or.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Research and Development, The Korean Institute of Tuberculosis, 168-5 Osongsaengmyeong4-ro, Heungdeok-gu, Cheongju-si, 28158, Chungcheongbuk-do</wicri:regionArea><wicri:noRegion>Chungcheongbuk-do</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Cheorl Ho" sort="Kim, Cheorl Ho" uniqKey="Kim C" first="Cheorl-Ho" last="Kim">Cheorl-Ho Kim</name><affiliation wicri:level="1"><nlm:affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea. chkimbio@skku.edu.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do</wicri:regionArea><wicri:noRegion>Kyunggi-do</wicri:noRegion></affiliation></author></analytic><series><title level="j">Inflammation</title><idno type="eISSN">1573-2576</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>Anti-Inflammatory Agents (pharmacology)</term><term>Antigens, Bacterial (pharmacology)</term><term>Bacterial Proteins (pharmacology)</term><term>Cell Movement (drug effects)</term><term>Cyclooxygenase 2 (metabolism)</term><term>Inflammation (chemically induced)</term><term>Inflammation (enzymology)</term><term>Inflammation (prevention & control)</term><term>Lipopolysaccharides (toxicity)</term><term>Macrophages (drug effects)</term><term>Macrophages (enzymology)</term><term>Matrix Metalloproteinase 9 (genetics)</term><term>Matrix Metalloproteinase 9 (metabolism)</term><term>Mice (MeSH)</term><term>Mitogen-Activated Protein Kinases (metabolism)</term><term>NF-kappa B (metabolism)</term><term>Nitric Oxide (metabolism)</term><term>Nitric Oxide Synthase Type II (metabolism)</term><term>Phosphorylation (MeSH)</term><term>RAW 264.7 Cells (MeSH)</term><term>Signal Transduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Anti-inflammatoires (pharmacologie)</term><term>Antigènes bactériens (pharmacologie)</term><term>Cellules RAW 264.7 (MeSH)</term><term>Cyclooxygenase 2 (métabolisme)</term><term>Facteur de transcription NF-kappa B (métabolisme)</term><term>Inflammation (enzymologie)</term><term>Inflammation (induit chimiquement)</term><term>Inflammation (prévention et contrôle)</term><term>Lipopolysaccharides (toxicité)</term><term>Macrophages (effets des médicaments et des substances chimiques)</term><term>Macrophages (enzymologie)</term><term>Matrix metalloproteinase 9 (génétique)</term><term>Matrix metalloproteinase 9 (métabolisme)</term><term>Mitogen-Activated Protein Kinases (métabolisme)</term><term>Monoxyde d'azote (métabolisme)</term><term>Mouvement cellulaire (effets des médicaments et des substances chimiques)</term><term>Nitric oxide synthase type II (métabolisme)</term><term>Phosphorylation (MeSH)</term><term>Protéines bactériennes (pharmacologie)</term><term>Souris (MeSH)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Matrix Metalloproteinase 9</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclooxygenase 2</term><term>Matrix Metalloproteinase 9</term><term>Mitogen-Activated Protein Kinases</term><term>NF-kappa B</term><term>Nitric Oxide</term><term>Nitric Oxide Synthase Type II</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Antigens, Bacterial</term><term>Bacterial Proteins</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Macrophages</term><term>Mouvement cellulaire</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Inflammation</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Inflammation</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Matrix metalloproteinase 9</term></keywords><keywords scheme="MESH" qualifier="induit chimiquement" xml:lang="fr"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cyclooxygenase 2</term><term>Facteur de transcription NF-kappa B</term><term>Matrix metalloproteinase 9</term><term>Mitogen-Activated Protein Kinases</term><term>Monoxyde d'azote</term><term>Nitric oxide synthase type II</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term><term>Antigènes bactériens</term><term>Protéines bactériennes</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Inflammation</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Lipopolysaccharides</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Lipopolysaccharides</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Phosphorylation</term><term>RAW 264.7 Cells</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules RAW 264.7</term><term>Phosphorylation</term><term>Souris</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">-20pt?>Mycobacterium tuberculosis (Mtb) is a pathogenic bacterium that causes contagious tuberculosis (TB). Recently, Mtb-secreted proteins have been considered virulence factors and candidates for drugs and vaccines. Among these proteins, 6-kDa early secreted antigenic target (ESAT-6) is known to be able to induce component of matrix metalloproteinase-9 (MMP-9) in epithelial cells, leading to recruitment of macrophages. However, detailed function of ESAT-6 during macrophage recruitment to inflammatory sites remains unknown. Thus, the objective of the present study was to elucidate such function of EAST-6 and mechanism(s) involved. In the present study, we have found that recombinant ESAT-6 purified in the form of ESAT-6 double-connected structure (2E6D) could inhibit lipopolysaccharide (LPS)-induced potential of cell migration and inflammation in murine macrophage cells. Interestingly, 2E6D suppressed LPS-induced MMP-9 expression at both protein and mRNA levels as well as its enzyme activity. Levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) enzymes as known upregulators of MMP-9 were significantly decreased when 2E6D has been treated. In addition, nitric oxide (NO) as a second messenger was also significantly decreased by treatment with the purified 2E6D. Furthermore, 2E6D inhibited LPS-induced phosphorylation of IκB and translocation of NF-κB. Moreover, 2E6D suppressed phosphorylation of MAPK signaling proteins. Taken together, these results suggest that ESAT-6 can suppress LPS-induced MMP-9 and inflammation by downregulating COX-2, iNOS, and NO through NF-κB and MAPK signaling.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31720987</PMID><DateCompleted><Year>2020</Year><Month>11</Month><Day>16</Day></DateCompleted><DateRevised><Year>2020</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1573-2576</ISSN><JournalIssue CitedMedium="Internet"><Volume>43</Volume><Issue>1</Issue><PubDate><Year>2020</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Inflammation</Title><ISOAbbreviation>Inflammation</ISOAbbreviation></Journal><ArticleTitle>Mycobacterium tuberculosis-Secreted Protein, ESAT-6, Inhibits Lipopolysaccharide-Induced MMP-9 Expression and Inflammation Through NF-κB and MAPK Signaling in RAW 264.7 Macrophage Cells.</ArticleTitle><Pagination><MedlinePgn>54-65</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10753-019-01087-x</ELocationID><Abstract><AbstractText>-20pt?>Mycobacterium tuberculosis (Mtb) is a pathogenic bacterium that causes contagious tuberculosis (TB). Recently, Mtb-secreted proteins have been considered virulence factors and candidates for drugs and vaccines. Among these proteins, 6-kDa early secreted antigenic target (ESAT-6) is known to be able to induce component of matrix metalloproteinase-9 (MMP-9) in epithelial cells, leading to recruitment of macrophages. However, detailed function of ESAT-6 during macrophage recruitment to inflammatory sites remains unknown. Thus, the objective of the present study was to elucidate such function of EAST-6 and mechanism(s) involved. In the present study, we have found that recombinant ESAT-6 purified in the form of ESAT-6 double-connected structure (2E6D) could inhibit lipopolysaccharide (LPS)-induced potential of cell migration and inflammation in murine macrophage cells. Interestingly, 2E6D suppressed LPS-induced MMP-9 expression at both protein and mRNA levels as well as its enzyme activity. Levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) enzymes as known upregulators of MMP-9 were significantly decreased when 2E6D has been treated. In addition, nitric oxide (NO) as a second messenger was also significantly decreased by treatment with the purified 2E6D. Furthermore, 2E6D inhibited LPS-induced phosphorylation of IκB and translocation of NF-κB. Moreover, 2E6D suppressed phosphorylation of MAPK signaling proteins. Taken together, these results suggest that ESAT-6 can suppress LPS-induced MMP-9 and inflammation by downregulating COX-2, iNOS, and NO through NF-κB and MAPK signaling.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ha</LastName><ForeName>Sun-Hyung</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Hyunju</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Jun-Young</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abekura</LastName><ForeName>Fukushi</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Young-Choon</ForeName><Initials>YC</Initials><AffiliationInfo><Affiliation>Faculty of Medicinal Biotechnology, Dong-A University, Busan, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Jeong-Ran</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Department of Research and Development, The Korean Institute of Tuberculosis, 168-5 Osongsaengmyeong4-ro, Heungdeok-gu, Cheongju-si, 28158, Chungcheongbuk-do, Republic of Korea. happyjrk@knta.or.kr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Cheorl-Ho</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>Molecular and Cellular Glycobiology Unit, Department of Biological Sciences, Sungkyunkwan University, Seoburo, Jangan-gu, 16419, Kyunggi-do, Republic of Korea. chkimbio@skku.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Inflammation</MedlineTA><NlmUniqueID>7600105</NlmUniqueID><ISSNLinking>0360-3997</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000942">Antigens, Bacterial</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C093276">ESAT-6 protein, Mycobacterium tuberculosis</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008070">Lipopolysaccharides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C440499">lipopolysaccharide, Escherichia coli O111 B4</NameOfSubstance></Chemical><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D052247">Nitric Oxide Synthase Type II</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="C496317">Nos2 protein, mouse</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 2.7.11.24</RegistryNumber><NameOfSubstance UI="D020928">Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.24.35</RegistryNumber><NameOfSubstance UI="D020780">Matrix Metalloproteinase 9</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.24.35</RegistryNumber><NameOfSubstance UI="C501830">Mmp9 protein, mouse</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000942" MajorTopicYN="N">Antigens, Bacterial</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051546" MajorTopicYN="N">Cyclooxygenase 2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020780" MajorTopicYN="N">Matrix Metalloproteinase 9</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020928" MajorTopicYN="N">Mitogen-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052247" MajorTopicYN="N">Nitric Oxide Synthase Type II</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000067996" MajorTopicYN="N">RAW 264.7 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ESAT-6</Keyword><Keyword MajorTopicYN="N">Mycobacterium tuberculosis</Keyword><Keyword MajorTopicYN="N">RAW 264.7 macrophage cells</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>11</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>11</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31720987</ArticleId><ArticleId IdType="doi">10.1007/s10753-019-01087-x</ArticleId><ArticleId IdType="pii">10.1007/s10753-019-01087-x</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Ha, Sun Hyung" sort="Ha, Sun Hyung" uniqKey="Ha S" first="Sun-Hyung" last="Ha">Sun-Hyung Ha</name></noRegion><name sortKey="Abekura, Fukushi" sort="Abekura, Fukushi" uniqKey="Abekura F" first="Fukushi" last="Abekura">Fukushi Abekura</name><name sortKey="Choi, Hyunju" sort="Choi, Hyunju" uniqKey="Choi H" first="Hyunju" last="Choi">Hyunju Choi</name><name sortKey="Kim, Cheorl Ho" sort="Kim, Cheorl Ho" uniqKey="Kim C" first="Cheorl-Ho" last="Kim">Cheorl-Ho Kim</name><name sortKey="Kim, Jeong Ran" sort="Kim, Jeong Ran" uniqKey="Kim J" first="Jeong-Ran" last="Kim">Jeong-Ran Kim</name><name sortKey="Lee, Young Choon" sort="Lee, Young Choon" uniqKey="Lee Y" first="Young-Choon" last="Lee">Young-Choon Lee</name><name sortKey="Park, Jun Young" sort="Park, Jun Young" uniqKey="Park J" first="Jun-Young" last="Park">Jun-Young Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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