gms | German Medical Science

German Congress of Orthopaedics and Traumatology (DKOU 2015)

20.10. - 23.10.2015, Berlin

Splenic neutrophil migration in a traumamodel with hemorrhagic shock in mice

Meeting Abstract

  • presenting/speaker Michel Teuben - Universitätsklinikum Utrecht, Klinik für Unfallchirurgie, Utrecht, Netherlands
  • Marjolein Heeres - Universitätsklinikum Utrecht, Klinik für Unfallchirurgie, Utrecht, Netherlands
  • Leon de Boer - Universitätsklinikum Utrecht, Klinik für Unfallchirurgie, Utrecht, Netherlands
  • Roman Pfeifer - Universitätsklinikum Aachen, Klinik für Unfallchirurgie, Aachen, Germany
  • Taco Blokhuis - Universitätsklinikum Utrecht, Klinik für Unfallchirurgie, Utrecht, Netherlands
  • Hans-Christoph Pape - Universitätsklinik und Poliklinik der RWTH Aachen, Klinik für Orthopädie und Unfallchirurgie, Schwerpunkt Unfallchirurgie, Aachen, Germany
  • Leo Koenderman - Universitätsklinikum Utrecht, Abteilung für Experimentelle Pneumologie, Utrecht, Netherlands
  • Luke Leenen - Universitätsklinikum Utrecht, Klinik für Unfallchirurgie, Utrecht, Netherlands

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2015). Berlin, 20.-23.10.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. DocGR17-1568

doi: 10.3205/15dkou495, urn:nbn:de:0183-15dkou4950

Published: October 5, 2015

© 2015 Teuben et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at



Objectives: Neutrophils (PMNs) are key effector cells in the immune response te trauma. Inadequate activation and deposition of these cells forms the basis for severe inflammatory complications such as ARDS and MODS. We recently identified different neutrophil phenotypes in blood of traumapatients. One subset of hypersegmented PMNs (CD16dim/CD62Lhigh), had in vitro T-cell suppressive capacities. As this suppressive effect requires direct cell-cell interactions, it is important to investigate where neutrophils co-localise with T cells in vivo. Literature showed in murine models of acute systemic inflammation that lipopolysaccharide (LPS) injection induces PMN homing in the spleen, as well as migration of PMNs into the splenic T-cell areas. Therefore, we hypothesized that in a traumamodel of hemorrhagic shock, PMNs co-localize with T-cells in the splenic white pulp.

Methods: A (BALB/c) mice model of hemorrhagic shock/resuscitation (HS/R) combined with a unilateral femur fracture was employed in this study. Mice were randomized into 5 groups: a control group, a 2 hours HS/R+femur fracture group, a 6 hour HS/R+femur fracture group and both a 2 and 6 hour sham group

As a positive control group we added a group of mice in which acute systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide. Splenic neutrophil localisation was determined by confocal microscopy and by flowcytometry. We used Ly6G/Gr-1 to identify PMNs, B220 for B-cells, CD3e for T-cells.

Results and Conclusion: Trauma with HS/R resulted in an increase of the absolute number of PMNs in the spleen after both 2 and 6 hours (P<0.05). However, co-localization of PMNs with T-cells in the splenic white pulp was not encountered in our trauma model. In the control group there was a virtual absence of PMNs in the splenic white pulp, whereas in the LPS-induced inflammation group migration of PMNs into the white pulp compartment was observed.

So in conclusion, similar to lipopolysaccharide induced inflammation, trauma with HS/R results in increased neutrophil homing in the spleen. However, in contrast to LPS, neutrophils do not migrate into the white pulp compartment. Therefore, it is unlikely that splenic neutrophil-T-cell interactions in the white pulp play a major role in immune dysregulation after trauma. Furthermore, we showed that various potentially suppressive subpopulations exist under different insult situations. The identification and characterization of neutrophil subpopulations will yield new insights to, and provide possible avenues for, the treatment of ARDS and MODS.