ArticleFrontiers in immunology2022
Platelet-Depletion of Whole Blood Reveals That Platelets Potentiate the Release of IL-8 From Leukocytes Into Plasma in a Thrombin-Dependent Manner.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Supernatants from stored platelet concentrates modulate the inflammatory response in platelet-depleted blood ex vivo.Frontiers in immunology · 2026Article
- Interleukin 8 as a Causal Link Between Aging and Impaired Influenza Antibody Responses in Older Adults.The Journal of infectious diseases · 2025Article
- Platelet signaling in immune landscape: comprehensive mechanism and clinical therapy.Biomarker research · 2024Review
- One immune cell to bind them all: platelet contribution to neurodegenerative disease.Molecular neurodegeneration · 2024Review
- Aberrant innate immune profile associated with COVID-19 mortality in Pretoria, South Africa.Clinical immunology (Orlando, Fla.) · 2024Article
- Storage of Transfusion Platelet Concentrates Is Associated with Complement Activation and Reduced Ability of Platelets to Respond to Protease-Activated Receptor-1 and Thromboxane A2 Receptor.International journal of molecular sciences · 2024Article
- The Inflammatory Response Induced by Aspergillus fumigatus Conidia Is Dependent on Complement Activation: Insight from a Whole Blood Model.Journal of innate immunity · 2024Article
- Platelet, a key regulator of innate and adaptive immunity.Frontiers in medicine · 2023Review
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: In a recent study, we found an elevated level of interleukin 8 (IL-8) in response to bacterial incubation in thrombin-sufficient human whole blood anticoagulated by the fibrin polymerization blocking peptide GPRP. Whether thrombin directly activated leukocytes or mediated the release Methods: We separated platelets from whole blood using a combination of 0.7% (w/v) citrate and GPRP for attenuating the hemostatic response during the separation of platelets. Cytokine responses were compared in whole blood and platelet-depleted blood upon Results: Platelets were not activated during the separation process but responded to stimuli upon re-calcification. Plasma levels of IL-1β, IL-1Ra, IL-6, IL-8, IP-10, MIP-1α, and MIP-1β were significantly reduced in platelet-depleted blood compared to whole blood, but recovered in the presence of platelets, or with the supernatant of activated platelets. The leukocyte fraction and platelets were each found to contribute to the elevation of IL-8 at around 5 ng/ml; however, if combined, the release of IL-8 increased to 26 ng/ml. This process was dependent on thrombin since the levels of IL-8 remained at 5 ng/ml in whole blood if thrombin was blocked. Intracellular staining revealed that monocytes were the main source for IL-8 expression. Conclusion: Our findings suggest that the release of IL-8 is mediated by the leukocytes, mainly monocytes, but potentiated
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