Platelet α-granules modulate the inflammatory response under systemic lipopolysaccharide injection in mice.
Identifieur interne : 000604 ( Main/Corpus ); précédent : 000603; suivant : 000605Platelet α-granules modulate the inflammatory response under systemic lipopolysaccharide injection in mice.
Auteurs : Sofiane Tariket ; Jose A. Guerrero ; Olivier Garraud ; Cedric Ghevaert ; Fabrice CognasseSource :
- Transfusion [ 1537-2995 ] ; 2019.
English descriptors
- KwdEn :
- Animals (MeSH), Blood Proteins (genetics), Blood Proteins (metabolism), CD40 Ligand (genetics), CD40 Ligand (metabolism), Disease Models, Animal (MeSH), Gray Platelet Syndrome (genetics), Gray Platelet Syndrome (immunology), Gray Platelet Syndrome (metabolism), Immunoassay (MeSH), Inflammation (chemically induced), Inflammation (genetics), Inflammation (immunology), Lipopolysaccharides (toxicity), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Mutation (genetics).
- MESH :
- chemical , genetics : Blood Proteins, CD40 Ligand.
- chemical , metabolism : Blood Proteins, CD40 Ligand.
- chemically induced : Inflammation.
- genetics : Gray Platelet Syndrome, Inflammation, Mutation.
- immunology : Gray Platelet Syndrome, Inflammation.
- metabolism : Gray Platelet Syndrome.
- chemical , toxicity : Lipopolysaccharides.
- Animals, Disease Models, Animal, Immunoassay, Male, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
BACKGROUND
Beyond their role in hemostasis and thrombosis, platelets are also important mediators of inflammation by the release of hundreds of factors stored in their α-granules. Mutations in Nbeal2 cause gray platelet syndrome (GPS), characterized by the lack of platelet α-granules. This study aims to evaluate the immunological (proinflammatory) effects of platelet α-granules.
STUDY DESIGN AND METHODS
We performed an experiment using Nbeal2
RESULTS
The lack of Nbeal2 (in Nbeal2
CONCLUSIONS
These results show that α-granules play a direct role in platelet-mediated inflammation balance, confirming the need to further investigate platelet-associated inflammatory pathophysiology and inflammatory adverse events related to blood transfusion.
DOI: 10.1111/trf.14970
PubMed: 30394544
Links to Exploration step
pubmed:30394544Le document en format XML
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<author><name sortKey="Tariket, Sofiane" sort="Tariket, Sofiane" uniqKey="Tariket S" first="Sofiane" last="Tariket">Sofiane Tariket</name>
<affiliation><nlm:affiliation>Université de Lyon, Groupe sur l'Immunité des Muqueuses et Agents Pathogènes (GIMAP)-EA3064, Saint-Etienne, France.</nlm:affiliation>
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<affiliation><nlm:affiliation>Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Etienne, France.</nlm:affiliation>
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<author><name sortKey="Guerrero, Jose A" sort="Guerrero, Jose A" uniqKey="Guerrero J" first="Jose A" last="Guerrero">Jose A. Guerrero</name>
<affiliation><nlm:affiliation>Department of Haematology, University of Cambridge and National Health Service (NHS) Blood and Transplant, Cambridge, United Kingdom.</nlm:affiliation>
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<affiliation><nlm:affiliation>National Health Service Blood and Transplant, Cambridge Biomedical Campus, Cambridge, United Kingdom.</nlm:affiliation>
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<author><name sortKey="Garraud, Olivier" sort="Garraud, Olivier" uniqKey="Garraud O" first="Olivier" last="Garraud">Olivier Garraud</name>
<affiliation><nlm:affiliation>Université de Lyon, Groupe sur l'Immunité des Muqueuses et Agents Pathogènes (GIMAP)-EA3064, Saint-Etienne, France.</nlm:affiliation>
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<affiliation><nlm:affiliation>Institut National de la Transfusion Sanguine, Paris, France.</nlm:affiliation>
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<author><name sortKey="Ghevaert, Cedric" sort="Ghevaert, Cedric" uniqKey="Ghevaert C" first="Cedric" last="Ghevaert">Cedric Ghevaert</name>
<affiliation><nlm:affiliation>Department of Haematology, University of Cambridge and National Health Service (NHS) Blood and Transplant, Cambridge, United Kingdom.</nlm:affiliation>
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<affiliation><nlm:affiliation>National Health Service Blood and Transplant, Cambridge Biomedical Campus, Cambridge, United Kingdom.</nlm:affiliation>
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<author><name sortKey="Cognasse, Fabrice" sort="Cognasse, Fabrice" uniqKey="Cognasse F" first="Fabrice" last="Cognasse">Fabrice Cognasse</name>
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<author><name sortKey="Garraud, Olivier" sort="Garraud, Olivier" uniqKey="Garraud O" first="Olivier" last="Garraud">Olivier Garraud</name>
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<affiliation><nlm:affiliation>Institut National de la Transfusion Sanguine, Paris, France.</nlm:affiliation>
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<author><name sortKey="Ghevaert, Cedric" sort="Ghevaert, Cedric" uniqKey="Ghevaert C" first="Cedric" last="Ghevaert">Cedric Ghevaert</name>
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<affiliation><nlm:affiliation>National Health Service Blood and Transplant, Cambridge Biomedical Campus, Cambridge, United Kingdom.</nlm:affiliation>
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<author><name sortKey="Cognasse, Fabrice" sort="Cognasse, Fabrice" uniqKey="Cognasse F" first="Fabrice" last="Cognasse">Fabrice Cognasse</name>
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<series><title level="j">Transfusion</title>
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<term>Blood Proteins (metabolism)</term>
<term>CD40 Ligand (genetics)</term>
<term>CD40 Ligand (metabolism)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Gray Platelet Syndrome (genetics)</term>
<term>Gray Platelet Syndrome (immunology)</term>
<term>Gray Platelet Syndrome (metabolism)</term>
<term>Immunoassay (MeSH)</term>
<term>Inflammation (chemically induced)</term>
<term>Inflammation (genetics)</term>
<term>Inflammation (immunology)</term>
<term>Lipopolysaccharides (toxicity)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Mutation (genetics)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Blood Proteins</term>
<term>CD40 Ligand</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Blood Proteins</term>
<term>CD40 Ligand</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Inflammation</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gray Platelet Syndrome</term>
<term>Inflammation</term>
<term>Mutation</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Gray Platelet Syndrome</term>
<term>Inflammation</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Gray Platelet Syndrome</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Lipopolysaccharides</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>Immunoassay</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Beyond their role in hemostasis and thrombosis, platelets are also important mediators of inflammation by the release of hundreds of factors stored in their α-granules. Mutations in Nbeal2 cause gray platelet syndrome (GPS), characterized by the lack of platelet α-granules. This study aims to evaluate the immunological (proinflammatory) effects of platelet α-granules.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>STUDY DESIGN AND METHODS</b>
</p>
<p>We performed an experiment using Nbeal2</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>The lack of Nbeal2 (in Nbeal2 </p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>These results show that α-granules play a direct role in platelet-mediated inflammation balance, confirming the need to further investigate platelet-associated inflammatory pathophysiology and inflammatory adverse events related to blood transfusion.</p>
</div>
</front>
</TEI>
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<Month>05</Month>
<Day>06</Day>
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<ArticleTitle>Platelet α-granules modulate the inflammatory response under systemic lipopolysaccharide injection in mice.</ArticleTitle>
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<Abstract><AbstractText Label="BACKGROUND">Beyond their role in hemostasis and thrombosis, platelets are also important mediators of inflammation by the release of hundreds of factors stored in their α-granules. Mutations in Nbeal2 cause gray platelet syndrome (GPS), characterized by the lack of platelet α-granules. This study aims to evaluate the immunological (proinflammatory) effects of platelet α-granules.</AbstractText>
<AbstractText Label="STUDY DESIGN AND METHODS">We performed an experiment using Nbeal2<sup>-/-</sup>
mice, the mouse model of GPS. Systemic inflammation was induced by intravenous injection of lipopolysaccharide (LPS). Inflammatory response was assessed by quantification of inflammatory soluble factors and platelet biological response modifiers.</AbstractText>
<AbstractText Label="RESULTS">The lack of Nbeal2 (in Nbeal2 <sup>-/-</sup>
mice, compared with controls) significantly reduced the recruitment of circulating neutrophils and monocytes. Moreover, after LPS injection, there was a significant increase in neutrophil and monocyte counts in control animals, compared with Nbeal2 <sup>-/-</sup>
mice. The control of inflammation, evaluated by the production of anti-inflammatory cytokines, appeared to be greater in Nbeal2<sup>-/-</sup>
mice compared with controls. Conversely, the production of certain inflammatory-soluble mediators known to characterize normal platelet secretion, such as soluble CD40 ligand (sCD40L), was decreased under experimental inflammation in Nbeal2 <sup>-/-</sup>
mice.</AbstractText>
<AbstractText Label="CONCLUSIONS">These results show that α-granules play a direct role in platelet-mediated inflammation balance, confirming the need to further investigate platelet-associated inflammatory pathophysiology and inflammatory adverse events related to blood transfusion.</AbstractText>
<CopyrightInformation>© 2018 AABB.</CopyrightInformation>
</Abstract>
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<ForeName>Sofiane</ForeName>
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<AffiliationInfo><Affiliation>Institut National de la Transfusion Sanguine, Paris, France.</Affiliation>
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<AffiliationInfo><Affiliation>National Health Service Blood and Transplant, Cambridge Biomedical Campus, Cambridge, United Kingdom.</Affiliation>
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<AffiliationInfo><Affiliation>Établissement Français du Sang Auvergne-Rhône-Alpes, Saint-Etienne, France.</Affiliation>
</AffiliationInfo>
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<Agency>British Heart Foundation</Agency>
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<Agency>Medical Research Council</Agency>
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