gms | German Medical Science

26. Jahrestagung der deutschsprachigen Arbeitsgemeinschaft für Verbrennungsbehandlung (DAV 2008)

06.01. bis 09.01.2008, Engelberg

Heat shock proteins seem to play a role in innate immunity intradermally potentially compensating for knocked-out lipopolysaccharide binding protein (LBP) in a partial thickness burn wound model

Meeting Abstract

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  • L. U. Lahoda - Universitätsklinik für Plastische, Hand und Wiederherstellungschirurgie, Verbrennungszentrum, Replantationszentrum, Medizinische Hochschule, Hannover
  • S. C. Wang - Universitätsklinik für Plastische, Hand und Wiederherstellungschirurgie, Verbrennungszentrum, Replantationszentrum, Medizinische Hochschule, Hannover
  • P. M. Vogt - Universitätsklinik für Plastische, Hand und Wiederherstellungschirurgie, Verbrennungszentrum, Replantationszentrum, Medizinische Hochschule, Hannover

DAV 2008. 26. Jahrestagung der deutschsprachigen Arbeitsgemeinschaft für Verbrennungsbehandlung. Engelberg, 06.-09.01.2008. Düsseldorf: German Medical Science GMS Publishing House; 2008. Doc08dav67

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dav2008/08dav67.shtml

Published: June 30, 2008

© 2008 Lahoda et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Background: Lipopolysaccharide-binding protein (LBP) is an integral part of the innate immune system’s response to Gram-negative bacteria. Heat shock proteins (HsPs) have proven lately to act as potent proinflammatory messengers and represent mediators of stress. Furthermore, heat shock proteins seem to be potent activators of the mononuclear cell line, as well as vascular cells. CD14 seems to be a receptor for both, heat shock proteins as well as LPS in formation with it´s receptor protein, LBP and therefore heat shock proteins and LBP seem to act agonistic. For our model we used C57Bl6 mice and there sisters, having had the LBP-gene knocked out and sustaining partial thickness burns.

Methods: Female wild-type C57BL6 mice and corresponding LBPkos received a 20% partial thickness burn wound. Using pooled GeneChip probe array (Affimetrix® gene chips) we screened for genes differentially expressed in the skin of the 2 strains of mice 6 hours postburn.

Results: GeneChip analysis (6 hrs postburn) showed that in addition to pro- and anti-inflammatory cytokines, several heat shock proteins (HsP 70 kDa (4, 3, 1) and HsP 110 kDa) showed at least a two-fold higher gene expression when LBP was missing in comparison to the control.

Conclusions: LBP plays a central role in activating the innate immune system in burns. Heat shock proteins are known to be quite unspecific “stress mediators” as well as activators of the mononuclear cell lines. According to our data they reveal a several fold increase in gene-expression levels when LBP is missing in a standardized partial thickness burn wound. Possibly a compensatory effect by heat shock proteins is found when LBP is absent as in our model.