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Platelet and Neutrophil Responses to Gram Positive Pathogens in Patients with Bacteremic Infection

Identifieur interne : 004521 ( Pmc/Curation ); précédent : 004520; suivant : 004522

Platelet and Neutrophil Responses to Gram Positive Pathogens in Patients with Bacteremic Infection

Auteurs : Daniel Johansson ; Oonagh Shannon ; Magnus Rasmussen

Source :

RBID : PMC:3226579

Abstract

Background

Many Gram-positive pathogens aggregate and activate platelets in vitro and this has been proposed to contribute to virulence. Platelets can also form complexes with neutrophils but little is however known about platelet and platelet-neutrophil responses in bacterial infection.

Methodology/Principal Findings

We added isolates of Gram-positive bacteria from 38 patients with a bacteremic infection to blood drawn from the same patient. Aggregometry and flow cytometry were used to assess platelet aggregation and to quantify activation of platelets, neutrophils, and platelet-neutrophils complexes (PNCs) induced by the bacteria. Fifteen healthy persons served as controls. Most isolates of Staphylococcus aureus, beta hemolytic streptococci, and Enterococcus faecalis induced aggregation of platelets from their respective hosts, whereas pneumococci failed to do so. S. aureus isolates induced platelet aggregation more rapidly in patients than in controls, whereas platelet activation by S. aureus was lower in patients than in controls. PNCs were more abundant in baseline samples from patients than in healthy controls and most bacterial isolates induced additional PNC formation and neutrophil activation.

Conclusion/Significance

We have demonstrated for the first time that bacteria isolated from patients with Gram-positive bacteremia can induce platelet activation and aggregation, PNC formation, and neutrophil activation in the same infected host. This underlines the significance of these interactions during infection, which could be a target for future therapies in sepsis.


Url:
DOI: 10.1371/journal.pone.0026928
PubMed: 22140434
PubMed Central: 3226579

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PMC:3226579

Le document en format XML

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<p>Many Gram-positive pathogens aggregate and activate platelets
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<title>Methodology/Principal Findings</title>
<p>We added isolates of Gram-positive bacteria from 38 patients with a bacteremic infection to blood drawn from the same patient. Aggregometry and flow cytometry were used to assess platelet aggregation and to quantify activation of platelets, neutrophils, and platelet-neutrophils complexes (PNCs) induced by the bacteria. Fifteen healthy persons served as controls. Most isolates of
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<p>We have demonstrated for the first time that bacteria isolated from patients with Gram-positive bacteremia can induce platelet activation and aggregation, PNC formation, and neutrophil activation in the same infected host. This underlines the significance of these interactions during infection, which could be a target for future therapies in sepsis.</p>
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<name sortKey="Orfanidou, A" uniqKey="Orfanidou A">A Orfanidou</name>
</author>
<author>
<name sortKey="Roussos, C" uniqKey="Roussos C">C Roussos</name>
</author>
<author>
<name sortKey="Christopoulou Kokkinou, V" uniqKey="Christopoulou Kokkinou V">V Christopoulou-Kokkinou</name>
</author>
</analytic>
</biblStruct>
<biblStruct>
<analytic>
<author>
<name sortKey=" Kesson, P" uniqKey=" Kesson P">P Åkesson</name>
</author>
<author>
<name sortKey="Cooney, J" uniqKey="Cooney J">J Cooney</name>
</author>
<author>
<name sortKey="Kishimoto, F" uniqKey="Kishimoto F">F Kishimoto</name>
</author>
<author>
<name sortKey="Bjorck, L" uniqKey="Bjorck L">L Björck</name>
</author>
</analytic>
</biblStruct>
</listBibl>
</div1>
</back>
</TEI>
<pmc article-type="research-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">PLoS One</journal-id>
<journal-id journal-id-type="publisher-id">plos</journal-id>
<journal-id journal-id-type="pmc">plosone</journal-id>
<journal-title-group>
<journal-title>PLoS ONE</journal-title>
</journal-title-group>
<issn pub-type="epub">1932-6203</issn>
<publisher>
<publisher-name>Public Library of Science</publisher-name>
<publisher-loc>San Francisco, USA</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">22140434</article-id>
<article-id pub-id-type="pmc">3226579</article-id>
<article-id pub-id-type="publisher-id">PONE-D-11-12942</article-id>
<article-id pub-id-type="doi">10.1371/journal.pone.0026928</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Research Article</subject>
</subj-group>
<subj-group subj-group-type="Discipline-v2">
<subject>Biology</subject>
<subj-group>
<subject>Microbiology</subject>
<subj-group>
<subject>Bacterial Pathogens</subject>
<subj-group>
<subject>Gram Positive</subject>
<subject>Staphylococci</subject>
<subject>Streptococci</subject>
</subj-group>
</subj-group>
<subj-group>
<subject>Immunity</subject>
<subj-group>
<subject>Innate Immunity</subject>
</subj-group>
</subj-group>
<subj-group>
<subject>Host-Pathogen Interaction</subject>
<subject>Medical Microbiology</subject>
</subj-group>
</subj-group>
</subj-group>
<subj-group subj-group-type="Discipline-v2">
<subject>Medicine</subject>
<subj-group>
<subject>Hematology</subject>
<subj-group>
<subject>Platelets</subject>
</subj-group>
</subj-group>
<subj-group>
<subject>Infectious Diseases</subject>
<subj-group>
<subject>Bacterial Diseases</subject>
<subj-group>
<subject>Bacteremia</subject>
<subject>Bloodstream Infections</subject>
<subject>Group A streptococcal infection</subject>
<subject>Pneumococcus</subject>
<subject>Staph Infections</subject>
<subject>Staphylococcus Aureus</subject>
</subj-group>
</subj-group>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>Platelet and Neutrophil Responses to Gram Positive Pathogens in Patients with Bacteremic Infection</article-title>
<alt-title alt-title-type="running-head">Platelet and Neutrophil Responses to Bacteremia</alt-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Johansson</surname>
<given-names>Daniel</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Shannon</surname>
<given-names>Oonagh</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Rasmussen</surname>
<given-names>Magnus</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
<xref ref-type="corresp" rid="cor1">
<sup>*</sup>
</xref>
</contrib>
</contrib-group>
<aff id="aff1">
<addr-line>Division of Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden</addr-line>
</aff>
<contrib-group>
<contrib contrib-type="editor">
<name>
<surname>Bereswill</surname>
<given-names>Stefan</given-names>
</name>
<role>Editor</role>
<xref ref-type="aff" rid="edit1"></xref>
</contrib>
</contrib-group>
<aff id="edit1">Charité-University Medicine Berlin, Germany</aff>
<author-notes>
<corresp id="cor1">* E-mail:
<email>Magnus.Rasmussen@med.lu.se</email>
</corresp>
<fn fn-type="con">
<p>Conceived and designed the experiments: MR OS DJ. Performed the experiments: DJ MR OS. Analyzed the data: DJ MR OS. Contributed reagents/materials/analysis tools: MR OS. Wrote the paper: MR DJ.</p>
</fn>
</author-notes>
<pub-date pub-type="collection">
<year>2011</year>
</pub-date>
<pub-date pub-type="epub">
<day>29</day>
<month>11</month>
<year>2011</year>
</pub-date>
<volume>6</volume>
<issue>11</issue>
<elocation-id>e26928</elocation-id>
<history>
<date date-type="received">
<day>6</day>
<month>7</month>
<year>2011</year>
</date>
<date date-type="accepted">
<day>6</day>
<month>10</month>
<year>2011</year>
</date>
</history>
<permissions>
<copyright-statement>Johansson et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</copyright-statement>
<copyright-year>2011</copyright-year>
</permissions>
<abstract>
<sec>
<title>Background</title>
<p>Many Gram-positive pathogens aggregate and activate platelets
<italic>in vitro</italic>
and this has been proposed to contribute to virulence. Platelets can also form complexes with neutrophils but little is however known about platelet and platelet-neutrophil responses in bacterial infection.</p>
</sec>
<sec>
<title>Methodology/Principal Findings</title>
<p>We added isolates of Gram-positive bacteria from 38 patients with a bacteremic infection to blood drawn from the same patient. Aggregometry and flow cytometry were used to assess platelet aggregation and to quantify activation of platelets, neutrophils, and platelet-neutrophils complexes (PNCs) induced by the bacteria. Fifteen healthy persons served as controls. Most isolates of
<italic>Staphylococcus aureus</italic>
, beta hemolytic streptococci, and
<italic>Enterococcus faecalis</italic>
induced aggregation of platelets from their respective hosts, whereas pneumococci failed to do so.
<italic>S. aureus</italic>
isolates induced platelet aggregation more rapidly in patients than in controls, whereas platelet activation by
<italic>S. aureus</italic>
was lower in patients than in controls. PNCs were more abundant in baseline samples from patients than in healthy controls and most bacterial isolates induced additional PNC formation and neutrophil activation.</p>
</sec>
<sec>
<title>Conclusion/Significance</title>
<p>We have demonstrated for the first time that bacteria isolated from patients with Gram-positive bacteremia can induce platelet activation and aggregation, PNC formation, and neutrophil activation in the same infected host. This underlines the significance of these interactions during infection, which could be a target for future therapies in sepsis.</p>
</sec>
</abstract>
<counts>
<page-count count="9"></page-count>
</counts>
</article-meta>
</front>
</pmc>
</record>

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