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Thrombin Differenti...
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Johnson, ChristinaUniv Oslo, Norway;RIKEN Oslo Univ Hosp, Norway
(author)
Thrombin Differentially Modulates the Acute Inflammatory Response to Escherichia coli and Staphylococcus aureus in Human Whole Blood
- Article/chapterEnglish2022
Publisher, publication year, extent ...
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2022-06-15
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American Association of Immunologists :AMER ASSOC IMMUNOLOGISTS,2022
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Numbers
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LIBRIS-ID:oai:DiVA.org:lnu-115623
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https://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-115623URI
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https://doi.org/10.4049/jimmunol.2101033DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Thrombin plays a central role in thromboinflammatory responses, but its activity is blocked in the common ex vivo human whole blood models, making an ex vivo study of thrombin effects on thromboinflammatory responses unfeasible. In this study, we exploited the anticoagulant peptide Gly-Pro-Arg-Pro (GPRP) that blocks fibrin polymerization to study the effects of thrombin on acute inflammation in response to Escherichia coli and Staphylococcus aureus. Human blood was anticoagulated with either GPRP or the thrombin inhibitor lepirudin and incubated with either E. coli or S. aureus for up to 4 h at 37 degrees C. In GPRP-anticoagulated blood, there were spontaneous elevations in thrombin levels and platelet activation, which further increased in the presence of bacteria. Complement activation and the expression of activation markers on monocytes and granulocytes increased to the same extent in both blood models in response to bacteria. Most cytokines were not elevated in response to thrombin alone, but thrombin presence substantially and heterogeneously modulated several cytokines that increased in response to bacterial incubations. Bacterial-induced releases of IL-8, MIP-1 alpha, and mip-1 beta were potentiated in the thrombin-active GPRP model, whereas the levels of IP-10, TNF, IL-6, and IL-1 beta were elevated in the thrombin-inactive lepirudin model. Complement CS-blockade, combined with CD14 inhibition, reduced the overall cytokine release significantly, both in thrombin-active and thrombin-inactive models. Our data support that thrombin itself marginally induces leukocyte-dependent cytokine release in this isolated human whole blood but is a significant modulator of bacteria-induced inflammation by a differential effect on cytokine patterns.
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Quach, Huy QuangUniv Oslo, Norway;RIKEN Oslo Univ Hosp, Norway
(author)
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Lau, CorinnaNordland Hosp, Norway
(author)
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Ekholt, KarinUniv Oslo, Norway;RIKEN Oslo Univ Hosp, Norway
(author)
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Espevik, TerjeNorwegian Univ Sci & Technol, Norway
(author)
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Woodruff, Trent M.Univ Queensland, Australia
(author)
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Pischke, Soren ErikUniv Oslo, Norway;RIKEN Oslo Univ Hosp, Norway
(author)
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Mollnes, Tom EirikUniv Oslo, Norway;RIKEN Oslo Univ Hosp, Norway;Nordland Hosp, Norway;Norwegian Univ Sci & Technol, Norway;Univ Tromso, Norway
(author)
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Nilsson, Per H.,1980-Linnéuniversitetet,Institutionen för kemi och biomedicin (KOB),Avancerade material,Univ Oslo, Norway;RIKEN Oslo Univ Hosp, Norway,Linnaeus Ctr Biomat Chem, BMC;HoRB(Swepub:lnu)enipe
(author)
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Univ Oslo, Norway;RIKEN Oslo Univ Hosp, NorwayNordland Hosp, Norway
(creator_code:org_t)
Related titles
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In:Journal of ImmunologyAmerican Association of Immunologists : AMER ASSOC IMMUNOLOGISTS208:12, s. 2771-27780022-17671550-6606
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Quach, Huy Quang
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Pischke, Soren E ...
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Linnaeus University