Document Detail


Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells.
MedLine Citation:
PMID:  18028369     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Ravi Maruvada; Anna M Blom; Nemani V Prasadarao
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2007-11-20
Journal Detail:
Title:  Immunology     Volume:  124     ISSN:  1365-2567     ISO Abbreviation:  Immunology     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-20     Completed Date:  2008-06-09     Revised Date:  2014-09-10    
Medline Journal Info:
Nlm Unique ID:  0374672     Medline TA:  Immunology     Country:  England    
Other Details:
Languages:  eng     Pagination:  265-76     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adult
Aging / immunology
Blood Bactericidal Activity
Brain / blood supply,  immunology,  microbiology
Complement C4b-Binding Protein
Complement Factor H / metabolism
Complement System Proteins / metabolism*
Endothelial Cells / immunology,  microbiology
Endothelium, Vascular / immunology,  microbiology
Escherichia coli / metabolism*,  pathogenicity
Fetal Blood / immunology
Histocompatibility Antigens / metabolism
Humans
Infant, Newborn
Phagocytosis
Streptococcus agalactiae / metabolism*,  pathogenicity
Virulence / immunology
Grant Support
ID/Acronym/Agency:
AI40567/AI/NIAID NIH HHS; R01 AI040567/AI/NIAID NIH HHS; R01 AI040567-13/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/C4BPA protein, human; 0/Complement C4b-Binding Protein; 0/Histocompatibility Antigens; 80295-65-4/Complement Factor H; 9007-36-7/Complement System Proteins
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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