Trauma-induced long-term alterations of human T cells and monocytes

• Verfasst von: Ruhrmann, Sophie [VerfasserIn]
• Verfasst von: Schneck, Emmanuel [VerfasserIn]
• Verfasst von: Markmann, Melanie [VerfasserIn]
• Verfasst von: Zink, Jan [VerfasserIn]
• Verfasst von: Zajonz, Thomas Simon [VerfasserIn]
• Verfasst von: Arens, Christoph [VerfasserIn]
• Verfasst von: Uhle, Florian [VerfasserIn]
• Verfasst von: Sander, Michael [VerfasserIn]
• Verfasst von: Koch, Christian [VerfasserIn]
• Titel: Trauma-induced long-term alterations of human T cells and monocytes
• Titelzusatz: results of an explorative, cross-sectional study
• Verf.angabe: Sophie Ruhrmann, Emmanuel Schneck, Melanie Markmann, Jan Zink, Thomas Simon Zajonz, Christoph Arens, Florian Uhle, Michael Sander, Christian Koch
• Jahr: 2020
• Umfang: 8 S.
• Fussnoten: Gesehen am 08.10.2020
• Titel Quelle: Enthalten in: Shock
• Ort Quelle: Hagerstown, Md. : Lippincott, Williams & Wilkins, 1994
• Jahr Quelle: 2020
• Band/Heft Quelle: 53(2020), 1, Seite 35-42
• ISSN Quelle: 1540-0514
• DOI: doi:10.1097/SHK.0000000000001358
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1735197955

Abstract

Background: Major trauma leads to complex immune reactions, known to result in a transient immunodeficiency. The long-term consequences of severe trauma on immune function and regulation as well as its clinical impact remain unclear. Methods: Six months (ranging from −12 to +5 days) after a major trauma event, 12 former trauma patients (Injury Severity Score ≥ 16) and 12 healthy volunteers were enrolled. The current clinical status and infection history since discharge were assessed by a standardized questionnaire. Immune cell subsets (cluster of differentiation (CD)4+, CD8+, CD14+), cell surface receptor expression (programmed cell death protein 1 (PD-1), B- and T-lymphocyte attenuator (BTLA), cytotoxic T-lymphocyte-associated protein 4, toll-like receptor (TLR)-2, -4, and -5, Dectin-1, programmed death ligand 1 (PD-1L)), and human leucocyte antigen D-related receptor (HLA-DR)-expression were quantified by flow cytometry. Cytokine secretion (IL-2, -4, -6, -10, and 17A, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ) was assessed after stimulation of whole blood with LPS-, α-CD3/28, or zymosan. Results: Analysis of surface receptors on T cells revealed a significant elevation of PD-1 expression on CD4+ T cells, whereas BTLA expression on CD4+ and CD8+ T cells was significantly suppressed in the trauma cohort. Monocytes showed a significantly reduced expression of TLR-2 and -4 as well as a reduced proportion of TLR-4 monocytes. HLA-DR receptor density revealed no significant changes between both cohorts. LPS-induced IL-6 and TNF-α secretion showed non-significant trends toward reduced values. No differences regarding clinical apparent infections could be detected. Conclusions: Six months following major trauma, changes of cell surface receptors on CD4+ and CD8+ T cells as well as on CD14+ monocytes were present, hinting toward an immunosuppressive phenotype. Following major trauma, although IL-6 and TNF-α release after stimulation were reduced, they did not reach statistical significance. Overall, further studies are necessary to evaluate the clinical implications of these findings.