AustralieFrV1, PubMed, Checkpoint, bibRecord, 003626

Endotoxin-induced monocytic microparticles have contrasting effects on endothelial inflammatory responses.

Identifieur interne : 003626 ( PubMed/Checkpoint ); précédent : 003625; suivant : 003627

Endotoxin-induced monocytic microparticles have contrasting effects on endothelial inflammatory responses.

Auteurs : Beryl Wen [Australie] ; Valery Combes [Australie] ; Amandine Bonhoure [Australie] ; Babette B. Weksler [États-Unis] ; Pierre-Olivier Couraud [France] ; Georges E R. Grau [Australie]

Source :

PloS one [ 1932-6203 ] ; 2014.

RBID : pubmed:24646764

Descripteurs français

English descriptors

KwdEn :
- Brain (cytology), Brain (drug effects), Brain (metabolism), Cell Line, Cell-Derived Microparticles (chemistry), Cell-Derived Microparticles (metabolism), Coculture Techniques, Endothelial Cells (cytology), Endothelial Cells (drug effects), Endothelial Cells (metabolism), Gene Expression, Humans, Inflammation (metabolism), Inflammation (pathology), Intercellular Adhesion Molecule-1 (genetics), Intercellular Adhesion Molecule-1 (metabolism), Interleukin-6 (genetics), Interleukin-6 (metabolism), Interleukin-8 (genetics), Interleukin-8 (metabolism), Lipopolysaccharides (pharmacology), Monocytes (cytology), Monocytes (drug effects), Monocytes (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), Signal Transduction, Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (metabolism).
MESH :
- chemical , genetics : Intercellular Adhesion Molecule-1, Interleukin-6, Interleukin-8, RNA, Messenger, Tumor Necrosis Factor-alpha.
- chemistry : Cell-Derived Microparticles.
- cytology : Brain, Endothelial Cells, Monocytes.
- drug effects : Brain, Endothelial Cells, Monocytes.
- metabolism : Brain, Cell-Derived Microparticles, Endothelial Cells, Inflammation, Intercellular Adhesion Molecule-1, Interleukin-6, Interleukin-8, Monocytes, RNA, Messenger, Tumor Necrosis Factor-alpha.
- pathology : Inflammation.
- chemical , pharmacology : Lipopolysaccharides.
- Cell Line, Coculture Techniques, Gene Expression, Humans, Signal Transduction.

Abstract

Septic shock is a severe disease state characterised by the body's life threatening response to infection. Complex interactions between endothelial cells and circulating monocytes are responsible for microvasculature dysfunction contributing to the pathogenesis of this syndrome. Here, we intended to determine whether microparticles derived from activated monocytes contribute towards inflammatory processes and notably vascular permeability. We found that endotoxin stimulation of human monocytes enhances the release of microparticles of varying phenotypes and mRNA contents. Elevated numbers of LPS-induced monocytic microparticles (mMP) expressed CD54 and contained higher levels of transcripts for pro-inflammatory cytokines such as TNF, IL-6 and IL-8. Using a prothrombin time assay, a greater reduction in plasma coagulation time was observed with LPS-induced mMP than with non-stimulated mMP. Co-incubation of mMP with the human brain endothelial cell line hCMEC/D3 triggered their time-dependent uptake and significantly enhanced endothelial microparticle release. Unexpectedly, mMP also modified signalling pathways by diminishing pSrc (tyr416) expression and promoted endothelial monolayer tightness, as demonstrated by endothelial impedance and permeability assays. Altogether, these data strongly suggest that LPS-induced mMP have contrasting effects on the intercellular communication network and display a dual potential: enhanced pro-inflammatory and procoagulant properties, together with protective function of the endothelium.

DOI: 10.1371/journal.pone.0091597
PubMed: 24646764

Affiliations:

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<front><div type="abstract" xml:lang="en">Septic shock is a severe disease state characterised by the body's life threatening response to infection. Complex interactions between endothelial cells and circulating monocytes are responsible for microvasculature dysfunction contributing to the pathogenesis of this syndrome. Here, we intended to determine whether microparticles derived from activated monocytes contribute towards inflammatory processes and notably vascular permeability. We found that endotoxin stimulation of human monocytes enhances the release of microparticles of varying phenotypes and mRNA contents. Elevated numbers of LPS-induced monocytic microparticles (mMP) expressed CD54 and contained higher levels of transcripts for pro-inflammatory cytokines such as TNF, IL-6 and IL-8. Using a prothrombin time assay, a greater reduction in plasma coagulation time was observed with LPS-induced mMP than with non-stimulated mMP. Co-incubation of mMP with the human brain endothelial cell line hCMEC/D3 triggered their time-dependent uptake and significantly enhanced endothelial microparticle release. Unexpectedly, mMP also modified signalling pathways by diminishing pSrc (tyr416) expression and promoted endothelial monolayer tightness, as demonstrated by endothelial impedance and permeability assays. Altogether, these data strongly suggest that LPS-induced mMP have contrasting effects on the intercellular communication network and display a dual potential: enhanced pro-inflammatory and procoagulant properties, together with protective function of the endothelium.</div>
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<Abstract><AbstractText>Septic shock is a severe disease state characterised by the body's life threatening response to infection. Complex interactions between endothelial cells and circulating monocytes are responsible for microvasculature dysfunction contributing to the pathogenesis of this syndrome. Here, we intended to determine whether microparticles derived from activated monocytes contribute towards inflammatory processes and notably vascular permeability. We found that endotoxin stimulation of human monocytes enhances the release of microparticles of varying phenotypes and mRNA contents. Elevated numbers of LPS-induced monocytic microparticles (mMP) expressed CD54 and contained higher levels of transcripts for pro-inflammatory cytokines such as TNF, IL-6 and IL-8. Using a prothrombin time assay, a greater reduction in plasma coagulation time was observed with LPS-induced mMP than with non-stimulated mMP. Co-incubation of mMP with the human brain endothelial cell line hCMEC/D3 triggered their time-dependent uptake and significantly enhanced endothelial microparticle release. Unexpectedly, mMP also modified signalling pathways by diminishing pSrc (tyr416) expression and promoted endothelial monolayer tightness, as demonstrated by endothelial impedance and permeability assays. Altogether, these data strongly suggest that LPS-induced mMP have contrasting effects on the intercellular communication network and display a dual potential: enhanced pro-inflammatory and procoagulant properties, together with protective function of the endothelium.</AbstractText>
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<tree><country name="Australie"><region name="Nouvelle-Galles du Sud"><name sortKey="Wen, Beryl" sort="Wen, Beryl" uniqKey="Wen B" first="Beryl" last="Wen">Beryl Wen</name>
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   |texte=   Endotoxin-induced monocytic microparticles have contrasting effects on endothelial inflammatory responses.
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	Serveur d'exploration sur les relations entre la France et l'Australie
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Endotoxin-induced monocytic microparticles have contrasting effects on endothelial inflammatory responses.

Endotoxin-induced monocytic microparticles have contrasting effects on endothelial inflammatory responses.

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