A rapid increase in macrophage-derived versican and hyaluronan in infectious lung disease.
Identifieur interne : 001039 ( Main/Exploration ); précédent : 001038; suivant : 001040A rapid increase in macrophage-derived versican and hyaluronan in infectious lung disease.
Auteurs : Mary Y. Chang [États-Unis] ; Yoshinori Tanino [Japon] ; Veronika Vidova [États-Unis] ; Michael G. Kinsella [États-Unis] ; Christina K. Chan [États-Unis] ; Pamela Y. Johnson [États-Unis] ; Thomas N. Wight [États-Unis] ; Charles W. Frevert [États-Unis]Source :
- Matrix biology : journal of the International Society for Matrix Biology [ 1569-1802 ] ; 2014.
Descripteurs français
- KwdFr :
- Acide hyaluronique (biosynthèse), Acide hyaluronique (métabolisme), Activation des macrophages (), Animaux, Escherichia coli (pathogénicité), Glucuronosyltransferase (biosynthèse), Humains, Immunité innée (), Immunité innée (génétique), Lipopolysaccharides (toxicité), Macrophages (), Macrophages (anatomopathologie), Maladies pulmonaires (anatomopathologie), Maladies pulmonaires (génétique), Poumon (), Poumon (anatomopathologie), Poumon (cytologie), Récepteur de type Toll-4 (génétique), Régulation de l'expression des gènes (), Souris, Versicanes (biosynthèse).
- MESH :
- anatomopathologie : Macrophages, Maladies pulmonaires, Poumon.
- biosynthèse : Acide hyaluronique, Glucuronosyltransferase, Versicanes.
- cytologie : Poumon.
- génétique : Immunité innée, Maladies pulmonaires, Récepteur de type Toll-4.
- métabolisme : Acide hyaluronique.
- pathogénicité : Escherichia coli.
- toxicité : Lipopolysaccharides.
- Activation des macrophages, Animaux, Humains, Immunité innée, Macrophages, Poumon, Régulation de l'expression des gènes, Souris.
English descriptors
- KwdEn :
- Animals, Escherichia coli (pathogenicity), Gene Expression Regulation (drug effects), Glucuronosyltransferase (biosynthesis), Humans, Hyaluronan Synthases, Hyaluronic Acid (biosynthesis), Hyaluronic Acid (metabolism), Immunity, Innate (drug effects), Immunity, Innate (genetics), Lipopolysaccharides (toxicity), Lung (cytology), Lung (drug effects), Lung (pathology), Lung Diseases (genetics), Lung Diseases (pathology), Macrophage Activation (drug effects), Macrophages (drug effects), Macrophages (pathology), Mice, Toll-Like Receptor 4 (genetics), Versicans (biosynthesis).
- MESH :
- chemical , biosynthesis : Glucuronosyltransferase, Hyaluronic Acid, Versicans.
- cytology : Lung.
- drug effects : Gene Expression Regulation, Immunity, Innate, Lung, Macrophage Activation, Macrophages.
- genetics : Immunity, Innate, Lung Diseases, Toll-Like Receptor 4.
- chemical , metabolism : Hyaluronic Acid.
- pathogenicity : Escherichia coli.
- pathology : Lung, Lung Diseases, Macrophages.
- chemical , toxicity : Lipopolysaccharides.
- Animals, Humans, Hyaluronan Synthases, Mice.
Abstract
The goals of this study were to characterize the changes in chondroitin sulfate proteoglycans and hyaluronan in lungs in acute response to gram-negative bacterial infection and to identify cellular components responsible for these changes. Mice were treated with intratracheal (IT) live Escherichia coli, E. coli lipopolysaccharide (LPS), or PBS. Both E. coli and LPS caused rapid selective increases in mRNA expression of versican and hyaluronan synthase (Has) isoforms 1 and 2 associated with increased immunohistochemical and histochemical staining for versican and hyaluronan in the lungs. Versican was associated with a subset of alveolar macrophages. To examine whether macrophages contribute to versican and hyaluronan accumulation, in vitro studies with primary cultures of bone marrow-derived and alveolar macrophages were performed. Unstimulated macrophages expressed very low levels of versican and hyaluronan synthase mRNA, with no detectible versican protein or hyaluronan product. Stimulation with LPS caused rapid increases in versican mRNA and protein, a rapid increase in Has1 mRNA, and concomitant inhibition of hyaluronidases 1 and 2, the major hyaluronan degrading enzymes. Hyaluronan could be detected following chloroquine pre-treatment, indicating rapid turnover and degradation of hyaluronan by macrophages. In addition, the effects of LPS, the M1 macrophage classical activation agonist, were compared to those of IL-4/IL-13 or IL-10, the M2a and M2c alternative activation agonists, respectively. Versican and Has1 increased only in response to M1 activation. Finally, the up-regulation of versican and Has1 in the whole lungs of wild-type mice following IT LPS was completely abrogated in TLR-4(-/-) mice. These findings suggest that versican and hyaluronan synthesis may play an important role in the innate immune response to gram-negative lung infection.
DOI: 10.1016/j.matbio.2014.01.011
PubMed: 24472738
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000304
- to stream PubMed, to step Curation: 000304
- to stream PubMed, to step Checkpoint: 000309
- to stream Ncbi, to step Merge: 000237
- to stream Ncbi, to step Curation: 000237
- to stream Ncbi, to step Checkpoint: 000237
- to stream Main, to step Merge: 001040
- to stream Main, to step Curation: 001039
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A rapid increase in macrophage-derived versican and hyaluronan in infectious lung disease.</title><author><name sortKey="Chang, Mary Y" sort="Chang, Mary Y" uniqKey="Chang M" first="Mary Y" last="Chang">Mary Y. Chang</name><affiliation wicri:level="2"><nlm:affiliation>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States. Electronic address: mychang@u.washington.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Tanino, Yoshinori" sort="Tanino, Yoshinori" uniqKey="Tanino Y" first="Yoshinori" last="Tanino">Yoshinori Tanino</name><affiliation wicri:level="1"><nlm:affiliation>Fukushima Medical University School of Medicine, Department of Pulmonary Medicine, Fukushima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Fukushima Medical University School of Medicine, Department of Pulmonary Medicine, Fukushima</wicri:regionArea><wicri:noRegion>Fukushima</wicri:noRegion></affiliation></author><author><name sortKey="Vidova, Veronika" sort="Vidova, Veronika" uniqKey="Vidova V" first="Veronika" last="Vidova">Veronika Vidova</name><affiliation wicri:level="2"><nlm:affiliation>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Kinsella, Michael G" sort="Kinsella, Michael G" uniqKey="Kinsella M" first="Michael G" last="Kinsella">Michael G. Kinsella</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Chan, Christina K" sort="Chan, Christina K" uniqKey="Chan C" first="Christina K" last="Chan">Christina K. Chan</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Johnson, Pamela Y" sort="Johnson, Pamela Y" uniqKey="Johnson P" first="Pamela Y" last="Johnson">Pamela Y. Johnson</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Wight, Thomas N" sort="Wight, Thomas N" uniqKey="Wight T" first="Thomas N" last="Wight">Thomas N. Wight</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Frevert, Charles W" sort="Frevert, Charles W" uniqKey="Frevert C" first="Charles W" last="Frevert">Charles W. Frevert</name><affiliation wicri:level="2"><nlm:affiliation>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States; Division of Pulmonary/Critical Care Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States; Division of Pulmonary/Critical Care Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24472738</idno><idno type="pmid">24472738</idno><idno type="doi">10.1016/j.matbio.2014.01.011</idno><idno type="wicri:Area/PubMed/Corpus">000304</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000304</idno><idno type="wicri:Area/PubMed/Curation">000304</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000304</idno><idno type="wicri:Area/PubMed/Checkpoint">000309</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000309</idno><idno type="wicri:Area/Ncbi/Merge">000237</idno><idno type="wicri:Area/Ncbi/Curation">000237</idno><idno type="wicri:Area/Ncbi/Checkpoint">000237</idno><idno type="wicri:Area/Main/Merge">001040</idno><idno type="wicri:Area/Main/Curation">001039</idno><idno type="wicri:Area/Main/Exploration">001039</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A rapid increase in macrophage-derived versican and hyaluronan in infectious lung disease.</title><author><name sortKey="Chang, Mary Y" sort="Chang, Mary Y" uniqKey="Chang M" first="Mary Y" last="Chang">Mary Y. Chang</name><affiliation wicri:level="2"><nlm:affiliation>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States. Electronic address: mychang@u.washington.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Tanino, Yoshinori" sort="Tanino, Yoshinori" uniqKey="Tanino Y" first="Yoshinori" last="Tanino">Yoshinori Tanino</name><affiliation wicri:level="1"><nlm:affiliation>Fukushima Medical University School of Medicine, Department of Pulmonary Medicine, Fukushima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Fukushima Medical University School of Medicine, Department of Pulmonary Medicine, Fukushima</wicri:regionArea><wicri:noRegion>Fukushima</wicri:noRegion></affiliation></author><author><name sortKey="Vidova, Veronika" sort="Vidova, Veronika" uniqKey="Vidova V" first="Veronika" last="Vidova">Veronika Vidova</name><affiliation wicri:level="2"><nlm:affiliation>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Kinsella, Michael G" sort="Kinsella, Michael G" uniqKey="Kinsella M" first="Michael G" last="Kinsella">Michael G. Kinsella</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Chan, Christina K" sort="Chan, Christina K" uniqKey="Chan C" first="Christina K" last="Chan">Christina K. Chan</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Johnson, Pamela Y" sort="Johnson, Pamela Y" uniqKey="Johnson P" first="Pamela Y" last="Johnson">Pamela Y. Johnson</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Wight, Thomas N" sort="Wight, Thomas N" uniqKey="Wight T" first="Thomas N" last="Wight">Thomas N. Wight</name><affiliation wicri:level="2"><nlm:affiliation>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Hope Heart Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Frevert, Charles W" sort="Frevert, Charles W" uniqKey="Frevert C" first="Charles W" last="Frevert">Charles W. Frevert</name><affiliation wicri:level="2"><nlm:affiliation>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States; Division of Pulmonary/Critical Care Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, WA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Comparative Pathology Program, Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, United States; Division of Pulmonary/Critical Care Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region></placeName></affiliation></author></analytic><series><title level="j">Matrix biology : journal of the International Society for Matrix Biology</title><idno type="eISSN">1569-1802</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Escherichia coli (pathogenicity)</term><term>Gene Expression Regulation (drug effects)</term><term>Glucuronosyltransferase (biosynthesis)</term><term>Humans</term><term>Hyaluronan Synthases</term><term>Hyaluronic Acid (biosynthesis)</term><term>Hyaluronic Acid (metabolism)</term><term>Immunity, Innate (drug effects)</term><term>Immunity, Innate (genetics)</term><term>Lipopolysaccharides (toxicity)</term><term>Lung (cytology)</term><term>Lung (drug effects)</term><term>Lung (pathology)</term><term>Lung Diseases (genetics)</term><term>Lung Diseases (pathology)</term><term>Macrophage Activation (drug effects)</term><term>Macrophages (drug effects)</term><term>Macrophages (pathology)</term><term>Mice</term><term>Toll-Like Receptor 4 (genetics)</term><term>Versicans (biosynthesis)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide hyaluronique (biosynthèse)</term><term>Acide hyaluronique (métabolisme)</term><term>Activation des macrophages ()</term><term>Animaux</term><term>Escherichia coli (pathogénicité)</term><term>Glucuronosyltransferase (biosynthèse)</term><term>Humains</term><term>Immunité innée ()</term><term>Immunité innée (génétique)</term><term>Lipopolysaccharides (toxicité)</term><term>Macrophages ()</term><term>Macrophages (anatomopathologie)</term><term>Maladies pulmonaires (anatomopathologie)</term><term>Maladies pulmonaires (génétique)</term><term>Poumon ()</term><term>Poumon (anatomopathologie)</term><term>Poumon (cytologie)</term><term>Récepteur de type Toll-4 (génétique)</term><term>Régulation de l'expression des gènes ()</term><term>Souris</term><term>Versicanes (biosynthèse)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Glucuronosyltransferase</term><term>Hyaluronic Acid</term><term>Versicans</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Macrophages</term><term>Maladies pulmonaires</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Acide hyaluronique</term><term>Glucuronosyltransferase</term><term>Versicanes</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation</term><term>Immunity, Innate</term><term>Lung</term><term>Macrophage Activation</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Immunity, Innate</term><term>Lung Diseases</term><term>Toll-Like Receptor 4</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Immunité innée</term><term>Maladies pulmonaires</term><term>Récepteur de type Toll-4</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hyaluronic Acid</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acide hyaluronique</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>Lung</term><term>Lung Diseases</term><term>Macrophages</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>Humans</term><term>Hyaluronan Synthases</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation des macrophages</term><term>Animaux</term><term>Humains</term><term>Immunité innée</term><term>Macrophages</term><term>Poumon</term><term>Régulation de l'expression des gènes</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The goals of this study were to characterize the changes in chondroitin sulfate proteoglycans and hyaluronan in lungs in acute response to gram-negative bacterial infection and to identify cellular components responsible for these changes. Mice were treated with intratracheal (IT) live Escherichia coli, E. coli lipopolysaccharide (LPS), or PBS. Both E. coli and LPS caused rapid selective increases in mRNA expression of versican and hyaluronan synthase (Has) isoforms 1 and 2 associated with increased immunohistochemical and histochemical staining for versican and hyaluronan in the lungs. Versican was associated with a subset of alveolar macrophages. To examine whether macrophages contribute to versican and hyaluronan accumulation, in vitro studies with primary cultures of bone marrow-derived and alveolar macrophages were performed. Unstimulated macrophages expressed very low levels of versican and hyaluronan synthase mRNA, with no detectible versican protein or hyaluronan product. Stimulation with LPS caused rapid increases in versican mRNA and protein, a rapid increase in Has1 mRNA, and concomitant inhibition of hyaluronidases 1 and 2, the major hyaluronan degrading enzymes. Hyaluronan could be detected following chloroquine pre-treatment, indicating rapid turnover and degradation of hyaluronan by macrophages. In addition, the effects of LPS, the M1 macrophage classical activation agonist, were compared to those of IL-4/IL-13 or IL-10, the M2a and M2c alternative activation agonists, respectively. Versican and Has1 increased only in response to M1 activation. Finally, the up-regulation of versican and Has1 in the whole lungs of wild-type mice following IT LPS was completely abrogated in TLR-4(-/-) mice. These findings suggest that versican and hyaluronan synthesis may play an important role in the innate immune response to gram-negative lung infection. </div></front></TEI><affiliations><list><country><li>Japon</li><li>États-Unis</li></country><region><li>Washington (État)</li></region></list><tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Chang, Mary Y" sort="Chang, Mary Y" uniqKey="Chang M" first="Mary Y" last="Chang">Mary Y. Chang</name></region><name sortKey="Chan, Christina K" sort="Chan, Christina K" uniqKey="Chan C" first="Christina K" last="Chan">Christina K. Chan</name><name sortKey="Frevert, Charles W" sort="Frevert, Charles W" uniqKey="Frevert C" first="Charles W" last="Frevert">Charles W. Frevert</name><name sortKey="Johnson, Pamela Y" sort="Johnson, Pamela Y" uniqKey="Johnson P" first="Pamela Y" last="Johnson">Pamela Y. Johnson</name><name sortKey="Kinsella, Michael G" sort="Kinsella, Michael G" uniqKey="Kinsella M" first="Michael G" last="Kinsella">Michael G. Kinsella</name><name sortKey="Vidova, Veronika" sort="Vidova, Veronika" uniqKey="Vidova V" first="Veronika" last="Vidova">Veronika Vidova</name><name sortKey="Wight, Thomas N" sort="Wight, Thomas N" uniqKey="Wight T" first="Thomas N" last="Wight">Thomas N. Wight</name></country><country name="Japon"><noRegion><name sortKey="Tanino, Yoshinori" sort="Tanino, Yoshinori" uniqKey="Tanino Y" first="Yoshinori" last="Tanino">Yoshinori Tanino</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001039 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001039 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:24472738
|texte= A rapid increase in macrophage-derived versican and hyaluronan in infectious lung disease.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:24472738" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |