Serveur d'exploration sur la rapamycine et les champignons

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Piperine metabolically regulates peritoneal resident macrophages to potentiate their functions against bacterial infection.

Identifieur interne : 000C43 ( Main/Exploration ); précédent : 000C42; suivant : 000C44

Piperine metabolically regulates peritoneal resident macrophages to potentiate their functions against bacterial infection.

Auteurs : Hao Pan [République populaire de Chine] ; Li-Hui Xu [République populaire de Chine] ; Mei-Yun Huang [République populaire de Chine] ; Qing-Bing Zha [République populaire de Chine] ; Gao-Xiang Zhao [République populaire de Chine] ; Xiao-Feng Hou [République populaire de Chine] ; Zi-Jian Shi [République populaire de Chine] ; Qiu-Ru Lin [République populaire de Chine] ; Dong-Yun Ouyang [République populaire de Chine] ; Xian-Hui He [République populaire de Chine]

Source :

RBID : pubmed:26439699

Descripteurs français

English descriptors

Abstract

Pepper, a daily-used seasoning for promoting appetite, is widely used in folk medicine for treating gastrointestinal diseases. Piperine is the major alkaloid in pepper and possesses a wide range of pharmacological activities. However, the mechanism for linking metabolic and medicinal activities of piperine remains unknown. Here we report that piperine robustly boosts mTORC1 activity by recruiting more system L1 amino acid transporter (SLC7A5/SLC3A2) to the cell membrane, thus promoting amino acid metabolism. Piperine-induced increase of mTORC1 activity in resident peritoneal macrophages (pMΦs) is correlated with enhanced production of IL-6 and TNF-α upon LPS stimulation. Such an enhancement of cytokine production could be abrogated by inhibitors of the mTOR signaling pathway, indicating mTOR's action in this process. Moreover, piperine treatment protected resident pMΦs from bacterium-induced apoptosis and disappearance, and increased their bacterial phagocytic ability. Consequently, piperine administration conferred mice resistance against bacterial infection and even sepsis. Our data highlight that piperine has the capacity to metabolically reprogram peritoneal resident macrophages to fortify their innate functions against bacterial infection.

DOI: 10.18632/oncotarget.5957
PubMed: 26439699
PubMed Central: PMC4741706


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Le document en format XML

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<term>Alkaloids (pharmacology)</term>
<term>Amino Acids (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Anti-Bacterial Agents (pharmacology)</term>
<term>Apoptosis (drug effects)</term>
<term>Benzodioxoles (pharmacology)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Escherichia coli (drug effects)</term>
<term>Escherichia coli (immunology)</term>
<term>Escherichia coli (pathogenicity)</term>
<term>Escherichia coli Infections (immunology)</term>
<term>Escherichia coli Infections (metabolism)</term>
<term>Escherichia coli Infections (microbiology)</term>
<term>Escherichia coli Infections (pathology)</term>
<term>Escherichia coli Infections (prevention & control)</term>
<term>Female (MeSH)</term>
<term>Fusion Regulatory Protein 1, Heavy Chain (metabolism)</term>
<term>HeLa Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Immunity, Innate (drug effects)</term>
<term>Inflammation Mediators (metabolism)</term>
<term>Interleukin-6 (metabolism)</term>
<term>Large Neutral Amino Acid-Transporter 1 (genetics)</term>
<term>Large Neutral Amino Acid-Transporter 1 (metabolism)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>Macrophage Activation (drug effects)</term>
<term>Macrophages, Peritoneal (drug effects)</term>
<term>Macrophages, Peritoneal (immunology)</term>
<term>Macrophages, Peritoneal (metabolism)</term>
<term>Macrophages, Peritoneal (microbiology)</term>
<term>Macrophages, Peritoneal (pathology)</term>
<term>Male (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Multiprotein Complexes (metabolism)</term>
<term>Phagocytosis (drug effects)</term>
<term>Piperidines (pharmacology)</term>
<term>Polyunsaturated Alkamides (pharmacology)</term>
<term>RAW 264.7 Cells (MeSH)</term>
<term>RNA Interference (MeSH)</term>
<term>Signal Transduction (drug effects)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Time Factors (MeSH)</term>
<term>Transfection (MeSH)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
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<term>Acides aminés (métabolisme)</term>
<term>Activation des macrophages (effets des médicaments et des substances chimiques)</term>
<term>Alcaloïdes (pharmacologie)</term>
<term>Amides gras polyinsaturés N-alkylés (pharmacologie)</term>
<term>Animaux (MeSH)</term>
<term>Antibactériens (pharmacologie)</term>
<term>Apoptose (effets des médicaments et des substances chimiques)</term>
<term>Benzodioxoles (pharmacologie)</term>
<term>Cellules HeLa (MeSH)</term>
<term>Cellules RAW 264.7 (MeSH)</term>
<term>Chaine lourde de l'antigène CD98 (métabolisme)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term>
<term>Complexes multiprotéiques (métabolisme)</term>
<term>Escherichia coli (effets des médicaments et des substances chimiques)</term>
<term>Escherichia coli (immunologie)</term>
<term>Escherichia coli (pathogénicité)</term>
<term>Facteur de nécrose tumorale alpha (métabolisme)</term>
<term>Facteurs temps (MeSH)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Immunité innée (effets des médicaments et des substances chimiques)</term>
<term>Infections à Escherichia coli (anatomopathologie)</term>
<term>Infections à Escherichia coli (immunologie)</term>
<term>Infections à Escherichia coli (microbiologie)</term>
<term>Infections à Escherichia coli (métabolisme)</term>
<term>Infections à Escherichia coli (prévention et contrôle)</term>
<term>Interférence par ARN (MeSH)</term>
<term>Interleukine-6 (métabolisme)</term>
<term>Lipopolysaccharides (pharmacologie)</term>
<term>Macrophages péritonéaux (anatomopathologie)</term>
<term>Macrophages péritonéaux (effets des médicaments et des substances chimiques)</term>
<term>Macrophages péritonéaux (immunologie)</term>
<term>Macrophages péritonéaux (microbiologie)</term>
<term>Macrophages péritonéaux (métabolisme)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Médiateurs de l'inflammation (métabolisme)</term>
<term>Phagocytose (effets des médicaments et des substances chimiques)</term>
<term>Pipéridines (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Transfection (MeSH)</term>
<term>Transporteur-1 d'acides aminés neutres à longue chaîne (génétique)</term>
<term>Transporteur-1 d'acides aminés neutres à longue chaîne (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en">
<term>Large Neutral Amino Acid-Transporter 1</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Amino Acids</term>
<term>Fusion Regulatory Protein 1, Heavy Chain</term>
<term>Inflammation Mediators</term>
<term>Interleukin-6</term>
<term>Large Neutral Amino Acid-Transporter 1</term>
<term>Multiprotein Complexes</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Tumor Necrosis Factor-alpha</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en">
<term>Alkaloids</term>
<term>Anti-Bacterial Agents</term>
<term>Benzodioxoles</term>
<term>Lipopolysaccharides</term>
<term>Piperidines</term>
<term>Polyunsaturated Alkamides</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr">
<term>Infections à Escherichia coli</term>
<term>Macrophages péritonéaux</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Apoptosis</term>
<term>Escherichia coli</term>
<term>Immunity, Innate</term>
<term>Macrophage Activation</term>
<term>Macrophages, Peritoneal</term>
<term>Phagocytosis</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr">
<term>Activation des macrophages</term>
<term>Apoptose</term>
<term>Escherichia coli</term>
<term>Immunité innée</term>
<term>Macrophages péritonéaux</term>
<term>Phagocytose</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Transporteur-1 d'acides aminés neutres à longue chaîne</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr">
<term>Escherichia coli</term>
<term>Infections à Escherichia coli</term>
<term>Macrophages péritonéaux</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>Escherichia coli</term>
<term>Escherichia coli Infections</term>
<term>Macrophages, Peritoneal</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Escherichia coli Infections</term>
<term>Macrophages, Peritoneal</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr">
<term>Infections à Escherichia coli</term>
<term>Macrophages péritonéaux</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Escherichia coli Infections</term>
<term>Macrophages, Peritoneal</term>
</keywords>
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<term>Acides aminés</term>
<term>Chaine lourde de l'antigène CD98</term>
<term>Complexes multiprotéiques</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Infections à Escherichia coli</term>
<term>Interleukine-6</term>
<term>Macrophages péritonéaux</term>
<term>Médiateurs de l'inflammation</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transporteur-1 d'acides aminés neutres à longue chaîne</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en">
<term>Escherichia coli</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr">
<term>Escherichia coli</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en">
<term>Escherichia coli Infections</term>
<term>Macrophages, Peritoneal</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr">
<term>Alcaloïdes</term>
<term>Amides gras polyinsaturés N-alkylés</term>
<term>Antibactériens</term>
<term>Benzodioxoles</term>
<term>Lipopolysaccharides</term>
<term>Pipéridines</term>
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<term>Escherichia coli Infections</term>
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<term>Infections à Escherichia coli</term>
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<term>Animals</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>HeLa Cells</term>
<term>Humans</term>
<term>Male</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>RAW 264.7 Cells</term>
<term>RNA Interference</term>
<term>Time Factors</term>
<term>Transfection</term>
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<keywords scheme="MESH" xml:lang="fr">
<term>Animaux</term>
<term>Cellules HeLa</term>
<term>Cellules RAW 264.7</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
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<front>
<div type="abstract" xml:lang="en">Pepper, a daily-used seasoning for promoting appetite, is widely used in folk medicine for treating gastrointestinal diseases. Piperine is the major alkaloid in pepper and possesses a wide range of pharmacological activities. However, the mechanism for linking metabolic and medicinal activities of piperine remains unknown. Here we report that piperine robustly boosts mTORC1 activity by recruiting more system L1 amino acid transporter (SLC7A5/SLC3A2) to the cell membrane, thus promoting amino acid metabolism. Piperine-induced increase of mTORC1 activity in resident peritoneal macrophages (pMΦs) is correlated with enhanced production of IL-6 and TNF-α upon LPS stimulation. Such an enhancement of cytokine production could be abrogated by inhibitors of the mTOR signaling pathway, indicating mTOR's action in this process. Moreover, piperine treatment protected resident pMΦs from bacterium-induced apoptosis and disappearance, and increased their bacterial phagocytic ability. Consequently, piperine administration conferred mice resistance against bacterial infection and even sepsis. Our data highlight that piperine has the capacity to metabolically reprogram peritoneal resident macrophages to fortify their innate functions against bacterial infection. </div>
</front>
</TEI>
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<DateCompleted>
<Year>2016</Year>
<Month>08</Month>
<Day>12</Day>
</DateCompleted>
<DateRevised>
<Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
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<Journal>
<ISSN IssnType="Electronic">1949-2553</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>6</Volume>
<Issue>32</Issue>
<PubDate>
<Year>2015</Year>
<Month>Oct</Month>
<Day>20</Day>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>Piperine metabolically regulates peritoneal resident macrophages to potentiate their functions against bacterial infection.</ArticleTitle>
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</Pagination>
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<Abstract>
<AbstractText>Pepper, a daily-used seasoning for promoting appetite, is widely used in folk medicine for treating gastrointestinal diseases. Piperine is the major alkaloid in pepper and possesses a wide range of pharmacological activities. However, the mechanism for linking metabolic and medicinal activities of piperine remains unknown. Here we report that piperine robustly boosts mTORC1 activity by recruiting more system L1 amino acid transporter (SLC7A5/SLC3A2) to the cell membrane, thus promoting amino acid metabolism. Piperine-induced increase of mTORC1 activity in resident peritoneal macrophages (pMΦs) is correlated with enhanced production of IL-6 and TNF-α upon LPS stimulation. Such an enhancement of cytokine production could be abrogated by inhibitors of the mTOR signaling pathway, indicating mTOR's action in this process. Moreover, piperine treatment protected resident pMΦs from bacterium-induced apoptosis and disappearance, and increased their bacterial phagocytic ability. Consequently, piperine administration conferred mice resistance against bacterial infection and even sepsis. Our data highlight that piperine has the capacity to metabolically reprogram peritoneal resident macrophages to fortify their innate functions against bacterial infection. </AbstractText>
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<Author ValidYN="Y">
<LastName>Pan</LastName>
<ForeName>Hao</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
</AffiliationInfo>
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<LastName>Xu</LastName>
<ForeName>Li-Hui</ForeName>
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<Affiliation>Department of Cell Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
</AffiliationInfo>
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<LastName>Huang</LastName>
<ForeName>Mei-Yun</ForeName>
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<Affiliation>Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
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<ForeName>Qing-Bing</ForeName>
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<Affiliation>Department of Fetal Medicine, the First Affiliated Hospital of Jinan University, Guangzhou, China.</Affiliation>
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<LastName>Zhao</LastName>
<ForeName>Gao-Xiang</ForeName>
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<Affiliation>Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
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<ForeName>Xiao-Feng</ForeName>
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<Affiliation>Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
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<ForeName>Qiu-Ru</ForeName>
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<Affiliation>Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
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<ForeName>Dong-Yun</ForeName>
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<Affiliation>Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
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<ForeName>Xian-Hui</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Immunobiology, College of Life Science and Technology, Jinan University, Guangzhou, China.</Affiliation>
</AffiliationInfo>
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<DescriptorName UI="D000596" MajorTopicYN="N">Amino Acids</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D000900" MajorTopicYN="N">Anti-Bacterial Agents</DescriptorName>
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</MeshHeading>
<MeshHeading>
<DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D052117" MajorTopicYN="N">Benzodioxoles</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004926" MajorTopicYN="N">Escherichia coli</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004927" MajorTopicYN="N">Escherichia coli Infections</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
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<MeshHeading>
<DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
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<DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D027283" MajorTopicYN="N">Large Neutral Amino Acid-Transporter 1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading>
<DescriptorName UI="D008070" MajorTopicYN="N">Lipopolysaccharides</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading>
<DescriptorName UI="D008262" MajorTopicYN="N">Macrophage Activation</DescriptorName>
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<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
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<name sortKey="Lin, Qiu Ru" sort="Lin, Qiu Ru" uniqKey="Lin Q" first="Qiu-Ru" last="Lin">Qiu-Ru Lin</name>
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