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Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells

Maruvada, Ravi; Blom, Anna LU and Prasadarao, Nemani V. (2008) In Immunology 124. p.265-276
Abstract
Escherichia coli K1 and Group B Streptococcus (GBS) are the most common bacteria that cause meningitis during the neonatal period. Complement, the first line of defence in the host, acts on these bacteria to opsonize with various components of complement for subsequent presentation to phagocytes. To counteract these opsonization effects, E. coli and GBS bind to the complement regulators C4 binding protein and Factor H, respectively. Nonetheless, the deposition of complement components on these two bacteria from neonatal serum and their effect on the host cell interaction is unclear. Here we demonstrated that the deposition of complement proteins from adult serum prevented the invasion of E. coli into human brain microvascular endothelial... (More)
Escherichia coli K1 and Group B Streptococcus (GBS) are the most common bacteria that cause meningitis during the neonatal period. Complement, the first line of defence in the host, acts on these bacteria to opsonize with various components of complement for subsequent presentation to phagocytes. To counteract these opsonization effects, E. coli and GBS bind to the complement regulators C4 binding protein and Factor H, respectively. Nonetheless, the deposition of complement components on these two bacteria from neonatal serum and their effect on the host cell interaction is unclear. Here we demonstrated that the deposition of complement proteins from adult serum prevented the invasion of E. coli into human brain microvascular endothelial cells, whereas the invasion of GBS was enhanced. In contrast, treatment with cord serum had no effect on the invasion of both these bacteria. We also examined the effect of the deposited complement proteins on phagocytosis using THP-1 cells and THP-1 cells differentiated into macrophages. Escherichia coli treated with adult serum neither attached nor entered these cells, whereas GBS was phagocytosed and survived efficiently. We further demonstrate that the inhibitory effect of complement proteins is the result of the bound complement inhibitors C4b-binding protein, in the case of E. coli, and Factor H, in the case of GBS. Taken together, these results suggest that E. coli and GBS utilize contrasting mechanisms of complement-mediated interactions with their target cells for successful establishment of disease. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
meningitis, invasion, endothelial cells, bacteria, complement
in
Immunology
volume
124
pages
265 - 276
publisher
Wiley-Blackwell
external identifiers
  • pmid:18028369
  • wos:000255924900013
  • scopus:43749101614
ISSN
0019-2805
DOI
10.1111/j.1365-2567.2007.02764.x
language
English
LU publication?
yes
id
4a858b3f-7212-485b-89cf-dc1f2139ef76 (old id 1138700)
date added to LUP
2008-04-29 09:07:40
date last changed
2017-08-27 03:58:24
@article{4a858b3f-7212-485b-89cf-dc1f2139ef76,
  abstract     = {Escherichia coli K1 and Group B Streptococcus (GBS) are the most common bacteria that cause meningitis during the neonatal period. Complement, the first line of defence in the host, acts on these bacteria to opsonize with various components of complement for subsequent presentation to phagocytes. To counteract these opsonization effects, E. coli and GBS bind to the complement regulators C4 binding protein and Factor H, respectively. Nonetheless, the deposition of complement components on these two bacteria from neonatal serum and their effect on the host cell interaction is unclear. Here we demonstrated that the deposition of complement proteins from adult serum prevented the invasion of E. coli into human brain microvascular endothelial cells, whereas the invasion of GBS was enhanced. In contrast, treatment with cord serum had no effect on the invasion of both these bacteria. We also examined the effect of the deposited complement proteins on phagocytosis using THP-1 cells and THP-1 cells differentiated into macrophages. Escherichia coli treated with adult serum neither attached nor entered these cells, whereas GBS was phagocytosed and survived efficiently. We further demonstrate that the inhibitory effect of complement proteins is the result of the bound complement inhibitors C4b-binding protein, in the case of E. coli, and Factor H, in the case of GBS. Taken together, these results suggest that E. coli and GBS utilize contrasting mechanisms of complement-mediated interactions with their target cells for successful establishment of disease.},
  author       = {Maruvada, Ravi and Blom, Anna and Prasadarao, Nemani V.},
  issn         = {0019-2805},
  keyword      = {meningitis,invasion,endothelial cells,bacteria,complement},
  language     = {eng},
  pages        = {265--276},
  publisher    = {Wiley-Blackwell},
  series       = {Immunology},
  title        = {Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells},
  url          = {http://dx.doi.org/10.1111/j.1365-2567.2007.02764.x},
  volume       = {124},
  year         = {2008},
}