Streptococcus agalactiae invasion of human brain microvascular endothelial cells is promoted by the laminin-binding protein Lmb

Tobias Tenenbaum, Barbara Spellerberg, Rüdiger Adam, Markus Vogel, Kwang Sik Kim, Horst Schroten

Research output: Contribution to journalArticlepeer-review

Abstract

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 colonizes and invades a number of host compartments, thereby interacting with different host tissues. Deletion of the scpB-lmb region, coding for the C5a peptidase and the laminin-binding protein Lmb, respectively, resulted in a 64% decreased invasion of S. agalactiae into human brain microvascular endothelial cells (HBMEC). Decreased invasion was also seen in lmb mutant strains lmb-k1 and lmb-k2 (74% and 69% reduction, respectively). Finally, host cell invasion was significantly reduced in competition experiments with either purified recombinant laminin-binding protein by 46% or a polyclonal antibody directed against the laminin-binding protein of S. agalactiae by 45%. The S. agalactiae scpB-lmb mutant induced an equal amount of the neutrophil chemoattractant interleukin (IL)-8 release in comparison to the wild-type. 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.

Original languageEnglish (US)
Pages (from-to)714-720
Number of pages7
JournalMicrobes and Infection
Volume9
Issue number6
DOIs
StatePublished - May 1 2007

Keywords

  • Group B streptococci
  • HBMEC
  • IL-8
  • Laminin-binding protein
  • Meningitis

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Infectious Diseases

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