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A role for C5 and C5a-ase in the acute neutrophil response to group B streptococcal infections.
J Infect Dis. 1997 Apr; 175(4):847-55.JI

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+Show Affiliations

Department of Pediatrics, University of Utah School of Medicine, Salt Lake City 84132, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9086140

Citation

Bohnsack, J F., et al. "A Role for C5 and C5a-ase in the Acute Neutrophil Response to Group B Streptococcal Infections." The Journal of Infectious Diseases, vol. 175, no. 4, 1997, pp. 847-55.
Bohnsack JF, Widjaja K, Ghazizadeh S, et al. A role for C5 and C5a-ase in the acute neutrophil response to group B streptococcal infections. J Infect Dis. 1997;175(4):847-55.
Bohnsack, J. F., Widjaja, K., Ghazizadeh, S., Rubens, C. E., Hillyard, D. R., Parker, C. J., Albertine, K. H., & Hill, H. R. (1997). A role for C5 and C5a-ase in the acute neutrophil response to group B streptococcal infections. The Journal of Infectious Diseases, 175(4), 847-55.
Bohnsack JF, et al. A Role for C5 and C5a-ase in the Acute Neutrophil Response to Group B Streptococcal Infections. J Infect Dis. 1997;175(4):847-55. PubMed PMID: 9086140.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A role for C5 and C5a-ase in the acute neutrophil response to group B streptococcal infections. AU - Bohnsack,J F, AU - Widjaja,K, AU - Ghazizadeh,S, AU - Rubens,C E, AU - Hillyard,D R, AU - Parker,C J, AU - Albertine,K H, AU - Hill,H R, PY - 1997/4/1/pubmed PY - 1997/4/1/medline PY - 1997/4/1/entrez SP - 847 EP - 55 JF - The Journal of infectious diseases JO - J Infect Dis VL - 175 IS - 4 N2 - 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. SN - 0022-1899 UR - https://www.unboundmedicine.com/medline/citation/9086140/A_role_for_C5_and_C5a_ase_in_the_acute_neutrophil_response_to_group_B_streptococcal_infections_ L2 - https://academic.oup.com/jid/article-lookup/doi/10.1086/513981 DB - PRIME DP - Unbound Medicine ER -