gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2023)

24. - 27.10.2023, Berlin

Altered expression of the adhesion GPCRs EMR2/ADGRE2 and CD97/ADGRE5 at circulating innate immune cells after traumatic injury

Meeting Abstract

  • presenting/speaker Leyu Zheng - University of Leipzig, Research Laboratory of Trauma, Leipzig, Germany
  • Moujie Rang - University of Leipzig, Research Laboratory of Trauma, Leipzig, Germany
  • Carolin Fuchs - University of Leipzig, Research Laboratory of Trauma, Leipzig, Germany
  • Cheng-Chih Hsiao - University of Amsterdam, Academic Medical Center, Amsterdam, Netherlands
  • Annette Keß - University of Leipzig, Research Laboratory of Trauma, Leipzig, Germany
  • Christian Kleber - University of Leipzig, Research Laboratory of Trauma, Leipzig, Germany
  • Georg Osterhoff - University of Leipzig, Research Laboratory of Trauma, Leipzig, Germany
  • Gabriela Aust - University of Leipzig, Research Laboratory of Trauma, Leipzig, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2023). Berlin, 24.-27.10.2023. Düsseldorf: German Medical Science GMS Publishing House; 2023. DocAB81-3178

doi: 10.3205/23dkou431, urn:nbn:de:0183-23dkou4311

Veröffentlicht: 23. Oktober 2023

© 2023 Zheng et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objectives: The time course and clinical outcome of severely injured patients are determined by the triggered inflammatory and compensatory anti-inflammatory and resolving immune responses. Innate immune cells provide a first line defense to the damage-associated molecular pattern (DAMP) released after major trauma. EMR2/ADGRE2 and CD97/ADGRE5, members of the Adhesion G protein-coupled receptor (aGPCR) family, are expressed at circulating neutrophils and monocytes und involved in their regulation.

Methods: Here, we monitored the expression of EMR2 and CD97 at circulating leukocytes of injured patients (injury severity score, ISS 9-75, n=34) up to 240 h after trauma by multicolor flow cytometry, and related the data to clinical and pathophysiological parameters of the patients.

Results and conclusion: The amount of immature neutrophils is higher in polytraumatized patients with an ISS >=25 (n=25) compared to less-injured patients (ISS <25; n=9) one and 8 h after injury. Interestingly, 8 h after trauma the percentage of EMR2+ classical and intermediate monocytes is decreased in patients with an ISS >=25, but not in less-injured patients. This early downregulation of EMR2 at monocytes correlates to increased levels of inflammatory cytokines. Further, the usually low percentage of EMR2+ mature neutrophilic granulocytes increased obviously 24–48 h and normalized 120–240 h after trauma. This characteristic time course was seen in almost all patients independent of the ISS, but not in healthy controls (n=5). In sum, aGPCR are regulated after polytraumatic injury at innate immune cells and are likely potential biomarkers for the patient's time course after trauma.