Abstract |
Congenic C5-deficient and C5-sufficient mice were infected with group B streptococci (GBS) to determine if the polymorphonuclear leukocyte (PMNL) chemoattractant C5a contributes to PMNL recruitment in GBS infection and if GBS C5a-ase reduces C5a-induced PMNL recruitment in vivo. PMNL accumulation was greater in the peritoneum and air spaces of C5-sufficient mice than in C5-deficient mice. Administration of human C5 to C5-deficient mice caused a significant increase in PMNL recruitment following infection with C5a-ase-negative GBS. GBS C5a-ase did not reduce PMNL accumulation in C5-sufficient mice but reduced PMNL recruitment in C5-deficient mice reconstituted with human C5. These data indicate that C5a is important for rapid PMNL recruitment to sites of GBS infection and that GBS C5a-ase inactivates human, but not murine, C5a in vivo. Reduction of the acute inflammatory response by C5a-ase likely contributes to GBS virulence in human neonates.
|
Authors | J F Bohnsack, K Widjaja, S Ghazizadeh, C E Rubens, D R Hillyard, C J Parker, K H Albertine, H R Hill |
Journal | The Journal of infectious diseases
(J Infect Dis)
Vol. 175
Issue 4
Pg. 847-55
(Apr 1997)
ISSN: 0022-1899 [Print] United States |
PMID | 9086140
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
|
Chemical References |
- Adhesins, Bacterial
- Complement C5
- Complement Inactivator Proteins
- Endopeptidases
- C5a peptidase
|
Topics |
- Adhesins, Bacterial
- Animals
- Complement C5
(physiology)
- Complement Inactivator Proteins
(physiology)
- Endopeptidases
(physiology)
- Humans
- Male
- Mice
- Neutrophils
(immunology)
- Streptococcal Infections
(immunology)
- Streptococcus agalactiae
(immunology)
|