The molecular mechanisms underlying entry of group B Streptococci (GBS) into human endothelial cells are not yet fully understood. This study is centered on the triggering of signaling cascade in human umbilical vein endothelial cells (HUVEC) during their interaction with different GBS serotypes/strains (type III: 80340-vagina and 90356-CSF and type V: 88641-vagina and 90186-blood). We have shown that the analyzed microorganisms adhere to HUVEC, but only those of the strains 90356-CSF, 88641-vagina and 90186-blood presented intracellular viability. Activation of PKC directly increased F-actin content and organization into stress fibers, and increased intracellular viability of GBS-III microorganisms. PKA inhibitor seems to promote surveillance of GBS type V microorganisms within HUVEC. These studies indicate that different molecules present at the cell surface of the GBS might induce different responses to HUVEC, interfering with the recruitment of cortical actin filaments.

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