Streptococcus agalactiae invasion of human brain microvascular endothelial cells is promoted by the laminin-binding protein
Abstract number: 1732_63
Tenenbaum T., Spellerberg B., Adam R., Vogel M., Kim K.S., Schroten H.
Objectives:Streptococcus agalactiae (S. agalactiae) can cause severe pneumonia, sepsis and meningitis in neonates and remains one of the most prevalent causes of invasive neonatal infections. During the course of infection, S. agalactiae colonises and invades a number of host compartments, thereby interacting with different host tissues. In this study, we investigated the role of S. agalactiae laminin-binding protein (Lmb) on adherence to and invasion of human brain microvascular endothelial cells (HBMEC).
Methods: In standard adherence and invasion assays we evaluated the capacity of scpB-lmb and lmb mutants of S. agalactiae to adhere to and invade into HBMEC and performed inhibition studies using wild-type S. agalactiae in combination with recombinant Lmb or polyclonal Lmb-antibodies. Furthermore interleukin (IL)-8 release was detected by ELISA.
Results: Deletion of the scpB-lmb region, coding for the C5a peptidase and Lmb, respectively, resulted in a decreased invasion of S. agalactiae into HBMEC. Decreased invasion was also seen in lmb mutant strains. Finally, host cell invasion was significantly blocked in competition experiments with either purified recombinant Lmb or a polyclonal antibody directed against the Lmb of S. agalactiae. The S. agalactiae scpB-lmb mutant induced an equal amount of the neutrophil chemoattractant IL-8 release in comparison to the wild-type.
Conclusion: Taken together, our studies support the conclusion that Lmb promotes invasion of S. agalactiae into HBMEC but does not play a role in IL-8 release from HBMEC.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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