gms | German Medical Science

64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

The role of S100B in inflammatory processes following traumatic brain injuries – preliminary results

Meeting Abstract

  • Marc Schwarz - Abteilung für Neurochirurgie, Universitätsklinikum Erlangen
  • Muhammed Nasir Khan - Abteilung für Neurochirurgie, Universitätsklinikum Erlangen
  • Michael Buchfelder - Abteilung für Neurochirurgie, Universitätsklinikum Erlangen
  • Andrea Kleindienst - Abteilung für Neurochirurgie, Universitätsklinikum Erlangen

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocMI.14.06

doi: 10.3205/13dgnc400, urn:nbn:de:0183-13dgnc4005

Published: May 21, 2013

© 2013 Schwarz et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Objective: The stimulated release of the calcium-binding glial protein S100B is known for its capability to enhance hippocampal neurogenesis and to improve cognitive recovery following traumatic brain injury (TBI). On the other hand, S100B may trigger microglial activation thereby contributing to neurodegeneration ultimatively resulting in Alsheimer's disease. In the present study, we investigate the participation of S100B in inflammatory processes following experimental TBI.

Method: Following lateral fluid percussion or sham injury in male Sprague-Dawley rats, S100B (50 ng/hr) or PBS was infused into the lateral ventricle for 7 days using osmotic micro-pumps. The animals were sacrificed on day 5 or 34 post-injury, and 5μm sections (distance 100 µm, bregma –3.3 to –5.6 mm) were analyzed histologically. The brain regional microglial/macrophage activation was quantified by immunostaining applying marker against CD68 (ED1) – a single chain membrane bound glycoprotein, CD11b – the α component of an integrin that mediates adhesion, and CD18 (IB4) – the β2 integrin of peripheral blood monocytes.

Results: Experimental TBI significantly increased the local expression of CD68 (day 5: bilateral subcortical area, ipsilateral CA3 region; day 34 ipsilateral subcortical area), CD11b (day 5: bilateral basal ganglia; day 34: corpus callosum and periventricular), and CD18 (day 5: periventricular; day 34: ipsilateral ventricle). While in sham animals, a S100B treatment enhanced the CD11b expression in the basal ganglia on day 5 and 34 (p=0.003 and p=0.046), the S100B effect on the microglial activation was more pronounced following injury. S100B increased the expression of CD68 (day 34: ipsilateral CA3 region, p=0.008; contralateral subcortical area, p=0.001, GCL, p<0.001, hilus, p=0.002), of CD11b (day 5: ipsilateral ventricle, p=0.006), and of CD18 (day 34: corpus callosum, p=0.004).

Conclusions: Our results demonstrate that S100B induces a microglial activation in the brain in non-injured and – even more pronounced – in injured animals. This effect is not limited to the lesion side, but also comprises a long-term effect in the contralateral hemisphere. Whether this participation in the brain neuroinflammatory response is beneficial or detrimental remains unclear. However, since we demonstrated earlier in the same animals that S100B augments significantly hippocampal neurogenesis and improves cognitive function, the S100B induced microglial activation does not counteract neuroregeneration within the first five weeks post-injury. Further studies are required to elucidate the respective cellular signalling and possible long-term effects.