Platelets modulate multiple markers of neutrophil function in response to in vitro Toll-like receptor stimulation
Identifieur interne : 000532 ( Main/Exploration ); précédent : 000531; suivant : 000533Platelets modulate multiple markers of neutrophil function in response to in vitro Toll-like receptor stimulation
Auteurs : Kathryn E. Hally [Nouvelle-Zélande] ; Georgina K. Bird [Nouvelle-Zélande] ; Anne C. La Flamme [Nouvelle-Zélande] ; Scott A. Harding [Nouvelle-Zélande] ; Peter D. Larsen [Nouvelle-Zélande]Source :
- PLoS ONE [ 1932-6203 ] ; 2019.
Abstract
In addition to their role in facilitating leukocyte-mediated inflammation, platelets can dampen leukocyte pro-inflammatory responses in some contexts. Consequently, platelets are increasingly appreciated as regulators of inflammation. Together, platelets and neutrophils play a role in inflammation through Toll-like receptor (TLR) expression, although we do not fully understand how platelets shape neutrophil responses to TLR stimulation. Here, we aimed to determine the extent to which platelets can modulate neutrophil function in response to
Neutrophils from 10 healthy individuals were cultured alone or with autologous platelets. Neutrophils ± platelets were left unstimulated or were stimulated with 1 or 100 ng/mL lipopolysaccharide (LPS; a TLR4 agonist), Pam3CSK4 (a TLR2/1 agonist) and fibroblast-stimulating lipopeptide (FSL)-1 (a TLR2/6 agonist). Neutrophil activation and phagocytic activity were assessed by flow cytometry, and elastase and interleukin-8 secretion were assessed by ELISA.
The addition of platelets attenuated neutrophil CD66b and CD11b expression in response to various doses of Pam3CSK4 and FSL-1. Furthermore, platelet co-culture was associated with higher CD62L expression (indicating reduced CD62L shedding) in response to these TLR agonists. Platelets also reduced elastase secretion in unstimulated cultures and in response to low-dose TLR stimulation. Conversely, platelet co-culture increased neutrophil phagocytosis in unstimulated cultures and in response to low-dose Pam3CSK4 and FSL-1. Platelets also increased IL-8 secretion in response to low-dose LPS.
Platelets are complex immunomodulators that can attenuate some, and simultaneously augment other, neutrophil functions. This modulation can occur both in the absence and presence of TLR stimulation.
Url:
DOI: 10.1371/journal.pone.0223444
PubMed: 31581214
PubMed Central: 6776355
Affiliations:
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Hally</name><affiliation wicri:level="1"><nlm:aff id="aff001"><addr-line>Department of Surgery and Anaesthesia, University of Otago, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Department of Surgery and Anaesthesia, University of Otago, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>School of Biological Sciences, Victoria University of Wellington, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff003"><addr-line>Wellington Cardiovascular Research Group, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Wellington Cardiovascular Research Group, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation></author><author><name sortKey="Bird, Georgina K" sort="Bird, Georgina K" uniqKey="Bird G" first="Georgina K." last="Bird">Georgina K. 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La Flamme</name><affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>School of Biological Sciences, Victoria University of Wellington, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff003"><addr-line>Wellington Cardiovascular Research Group, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Wellington Cardiovascular Research Group, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation></author><author><name sortKey="Harding, Scott A" sort="Harding, Scott A" uniqKey="Harding S" first="Scott A." last="Harding">Scott A. Harding</name><affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>School of Biological Sciences, Victoria University of Wellington, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff003"><addr-line>Wellington Cardiovascular Research Group, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Wellington Cardiovascular Research Group, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff004"><addr-line>Department of Cardiology, Wellington Hospital, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Department of Cardiology, Wellington Hospital, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation></author><author><name sortKey="Larsen, Peter D" sort="Larsen, Peter D" uniqKey="Larsen P" first="Peter D." last="Larsen">Peter D. Larsen</name><affiliation wicri:level="1"><nlm:aff id="aff001"><addr-line>Department of Surgery and Anaesthesia, University of Otago, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Department of Surgery and Anaesthesia, University of Otago, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>School of Biological Sciences, Victoria University of Wellington, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff003"><addr-line>Wellington Cardiovascular Research Group, Wellington, New Zealand</addr-line></nlm:aff><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Wellington Cardiovascular Research Group, Wellington</wicri:regionArea><wicri:noRegion>Wellington</wicri:noRegion></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="sec001"><title>Introduction</title><p>In addition to their role in facilitating leukocyte-mediated inflammation, platelets can dampen leukocyte pro-inflammatory responses in some contexts. Consequently, platelets are increasingly appreciated as regulators of inflammation. Together, platelets and neutrophils play a role in inflammation through Toll-like receptor (TLR) expression, although we do not fully understand how platelets shape neutrophil responses to TLR stimulation. Here, we aimed to determine the extent to which platelets can modulate neutrophil function in response to <italic>in vitro</italic> stimulation with TLR4, TLR2/1, and TLR2/6 agonists.</p></sec><sec id="sec002"><title>Methods</title><p>Neutrophils from 10 healthy individuals were cultured alone or with autologous platelets. Neutrophils ± platelets were left unstimulated or were stimulated with 1 or 100 ng/mL lipopolysaccharide (LPS; a TLR4 agonist), Pam3CSK4 (a TLR2/1 agonist) and fibroblast-stimulating lipopeptide (FSL)-1 (a TLR2/6 agonist). Neutrophil activation and phagocytic activity were assessed by flow cytometry, and elastase and interleukin-8 secretion were assessed by ELISA.</p></sec><sec id="sec003"><title>Results</title><p>The addition of platelets attenuated neutrophil CD66b and CD11b expression in response to various doses of Pam3CSK4 and FSL-1. Furthermore, platelet co-culture was associated with higher CD62L expression (indicating reduced CD62L shedding) in response to these TLR agonists. Platelets also reduced elastase secretion in unstimulated cultures and in response to low-dose TLR stimulation. Conversely, platelet co-culture increased neutrophil phagocytosis in unstimulated cultures and in response to low-dose Pam3CSK4 and FSL-1. Platelets also increased IL-8 secretion in response to low-dose LPS.</p></sec><sec id="sec004"><title>Conclusion</title><p>Platelets are complex immunomodulators that can attenuate some, and simultaneously augment other, neutrophil functions. This modulation can occur both in the absence and presence of TLR stimulation.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Yeaman, Mr" uniqKey="Yeaman M">MR Yeaman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Clark, Sr" uniqKey="Clark S">SR Clark</name></author><author><name sortKey="Ma, Ac" uniqKey="Ma A">AC Ma</name></author><author><name sortKey="Tavener, Sa" uniqKey="Tavener S">SA Tavener</name></author><author><name sortKey="Mcdonald, B" uniqKey="Mcdonald B">B McDonald</name></author><author><name sortKey="Goodarzi, Z" uniqKey="Goodarzi Z">Z Goodarzi</name></author><author><name sortKey="Kelly, Mm" uniqKey="Kelly M">MM Kelly</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Verschoor, A" uniqKey="Verschoor A">A Verschoor</name></author><author><name sortKey="Neuenhahn, M" uniqKey="Neuenhahn M">M Neuenhahn</name></author><author><name 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sortKey="Hultenby, K" uniqKey="Hultenby K">K Hultenby</name></author><author><name sortKey="Zhu, L" uniqKey="Zhu L">L Zhu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pokrovskaya, Id" uniqKey="Pokrovskaya I">ID Pokrovskaya</name></author><author><name sortKey="Aronova, Ma" uniqKey="Aronova M">MA Aronova</name></author><author><name sortKey="Kamykowski, Ja" uniqKey="Kamykowski J">JA Kamykowski</name></author><author><name sortKey="Prince, Aa" uniqKey="Prince A">AA Prince</name></author><author><name sortKey="Hoyne, Jd" uniqKey="Hoyne J">JD Hoyne</name></author><author><name sortKey="Calco, Gn" uniqKey="Calco G">GN Calco</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Nouvelle-Zélande</li></country></list><tree><country name="Nouvelle-Zélande"><noRegion><name sortKey="Hally, Kathryn E" sort="Hally, Kathryn E" uniqKey="Hally K" first="Kathryn E." last="Hally">Kathryn E. Hally</name></noRegion><name sortKey="Bird, Georgina K" sort="Bird, Georgina K" uniqKey="Bird G" first="Georgina K." last="Bird">Georgina K. Bird</name><name sortKey="Bird, Georgina K" sort="Bird, Georgina K" uniqKey="Bird G" first="Georgina K." last="Bird">Georgina K. Bird</name><name sortKey="Hally, Kathryn E" sort="Hally, Kathryn E" uniqKey="Hally K" first="Kathryn E." last="Hally">Kathryn E. Hally</name><name sortKey="Hally, Kathryn E" sort="Hally, Kathryn E" uniqKey="Hally K" first="Kathryn E." last="Hally">Kathryn E. Hally</name><name sortKey="Harding, Scott A" sort="Harding, Scott A" uniqKey="Harding S" first="Scott A." last="Harding">Scott A. Harding</name><name sortKey="Harding, Scott A" sort="Harding, Scott A" uniqKey="Harding S" first="Scott A." last="Harding">Scott A. Harding</name><name sortKey="Harding, Scott A" sort="Harding, Scott A" uniqKey="Harding S" first="Scott A." last="Harding">Scott A. Harding</name><name sortKey="La Flamme, Anne C" sort="La Flamme, Anne C" uniqKey="La Flamme A" first="Anne C." last="La Flamme">Anne C. La Flamme</name><name sortKey="La Flamme, Anne C" sort="La Flamme, Anne C" uniqKey="La Flamme A" first="Anne C." last="La Flamme">Anne C. La Flamme</name><name sortKey="Larsen, Peter D" sort="Larsen, Peter D" uniqKey="Larsen P" first="Peter D." last="Larsen">Peter D. Larsen</name><name sortKey="Larsen, Peter D" sort="Larsen, Peter D" uniqKey="Larsen P" first="Peter D." last="Larsen">Peter D. Larsen</name><name sortKey="Larsen, Peter D" sort="Larsen, Peter D" uniqKey="Larsen P" first="Peter D." last="Larsen">Peter D. Larsen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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