Platelets modulate multiple markers of neutrophil function in response to in vitro Toll-like receptor stimulation

English version

Autoři: Kathryn E. Hally ^aff001; Georgina K. Bird ^aff002; Anne C. La Flamme ^aff002; Scott A. Harding ^aff002; Peter D. Larsen ^aff001
Působiště autorů: Department of Surgery and Anaesthesia, University of Otago, Wellington, New Zealand ^aff001; School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand ^aff002; Wellington Cardiovascular Research Group, Wellington, New Zealand ^aff003; Department of Cardiology, Wellington Hospital, Wellington, New Zealand ^aff004
Vyšlo v časopise: PLoS ONE 14(10)
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pone.0223444

Souhrn

Introduction

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 in vitro stimulation with TLR4, TLR2/1, and TLR2/6 agonists.

Methods

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.

Results

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.

Conclusion

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.

Klíčová slova:

Inflammation – Inflammatory diseases – Neutrophils – Phagocytosis – Platelet activation – Platelets – Secretion – Toll-like receptors

Zdroje

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Platelets modulate multiple markers of neutrophil function in response to in vitro Toll-like receptor stimulation

Souhrn

Introduction

Methods

Results

Conclusion

Klíčová slova:

Zdroje

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