Abstract
Background: Group B Streptococcal infection is still the most common cause of neonatal sepsis in industrial countries. Activation of the platelet FcgammaRII-receptor (CD32) leads to platelet activation, aggregation and secretion, being tightly regulated by intracellular signalling pathways. Expression of inflammatory markers, e.g. P-selectin (CD62p) on activated platelets promotes adhesion of leucocytes to endothelial lesions and induces inflammatory reactions. We examined the molecular and functional effects of the direct interaction between platelets and Group B Streptococci (GBS).
Methods: Platelet-rich plasma was incubated with septic or non-septic strains in the presence or absence of FcgammaRII-receptor-blocking antibodies. Platelet aggregation was measured with PAP3-aggregometer (BioData). Activation of intracellular signalling pathways (PhospholipaseCgammaII (PLCgammaII), Calcium/Calmodulin-dependent proteinkinase II (CaMKII) and Myosin-light-chain-kinase 2 (MLC2)) was evaluated by western-blot-analysis. CD62p-expression was measured by flow cytometry.
Results: The septic strains induced rapid and full platelet aggregation (mean lag time until full aggregation: 5 min, range 2–8 min) while there was no aggregation after incubation with the non-septic strain. Incubation of platelets with the septic strains and to a lesser extent the non-septic strain lead to activation of PLCgammaII, CaMKII und MLC2; activation could be blocked by preincubation with anti-FcgammaRII-receptor-blocking antibodies. Incubation of platelets with the septic strains lead to a significant increase in P-selectin-expression (p< 0,05), while incubation with the non-septic strain (p=0,976) did not have any effect on CD62-expression in platelets.
Conclusions: In our experiments platelets incubated with the septic GBS-strains were activated, while incubation with the non-septic strain did only have little or no effect on platelet function. There seem to be different potentials to activate platelets in different GBS-strains. Group B streptococci seem to influence not only hemostasis but also inflammatory reactions in the setting of a possible septic event.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Siauw, C., Kobsar, A., Schubert-Unkmeier, A. et al. 349 Streptococcus Agalactiae Interacts with Human Platelets by Activating the Fcgammarii-Receptor and Promoting CD62-Expression. Pediatr Res 58, 414 (2005). https://doi.org/10.1203/00006450-200508000-00378
Issue Date:
DOI: https://doi.org/10.1203/00006450-200508000-00378