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Meeting abstract

High mortality rates days or weeks after multiple injury are often due to multiple organ dysfunction (MODS). Recent studies put a close view to the course of immunological mediators as the members of the selectin family to figure out their contribution to shock, sepsis and organ failure [1]. Brain contusion is supposed to cause cellular infiltrates and inflammation in brain tissue [2].

P-selectin (CD62P) is stored in endothelial cells (EC) Wiebel-Palade-bodies and in thrombocytes. It is rapidly released after cell activation. E-selectin (CD62E) is expressed on the cell surface of EC and shed from there after IL-1/TNF stimulation. L-selectin (CD62L) can be found on the surface of leukocytes. Cell activation leads to shed L-selectin by proteolytic processes [3].

We examined soluble E- and P-selectin and L-selectin on B-lymphocytes in multiple injured patients without or with moderate or with severe head injury. The classification of head injury was performed following the injury severity score (ISS) (0-2 pts, moderate; 3-5 pts, severe head injury).

sE-, P- and L-selectin were- measured in 51 multiple injured patients with samples taken on 10 time points (from the location of the accident = 0 h to the 6th post-traumatic day = 144 h) by using commercially available standardized enzyme-linked immunoassays (ELISA). CD62L levels on leukocyte subpopulations were detected using the monoclonal antibodies CD62L (LECAM-1), CD3 (T-cell), CD19 (B-cell), CD14 (monocyte) and a standard flow cytometer.

Table 1 demonstrates the very early increase of sP-selectin in patients with severe head injury (P = 0.0001) compared to those with moderate or no head injury.

Table 2 illustrates the later increase (P = 0.0026) of sL-selectin levels (72 h) in severe head injured individuals while L-selectin on CD19+ B-lymphocytes is expressed significantly stronger (P = 0.0001) in the very early post-traumatic phase (0-24 h) = Table 3.

The gravity of head trauma seems to influence the immunological response and subsequently the cell-cell interactions.

Acknowledgement

Supported by the BMVg, Grant InSan 1 0993-V-1296.

References

1. Gearing AH, Newman W: Circulating adhesion molecules in disease.

   Immunology Today 1993, 14:506-512. PubMed Abstract | Publisher Full Text

2. Holmin S, Mathiesen T, Shetye J, Biberfeld P: Intracerebral inflammatory response to experimental brain contusion.

   Acta Neurochirurgica 1995, 132:110-119. PubMed Abstract | Publisher Full Text

3. Redl H, Nikolai A, Kneidinger R, Schlag G: Endothelial and leukocyte activation in experimental polytrauma and sepsis.

   Behring Inst Mitt 1993, 92:218-228. PubMed Abstract

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