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J Infect Dis. 2009 Apr 15;199(8):1233-8. doi: 10.1086/597425.

A 28-aa pneumococcal surface adhesin A-derived peptide, P4, augments passive immunotherapy and rescues mice from fatal pneumococcal infection.

Author information

1
Division of Bacterial Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.

Abstract

BACKGROUND:

P4, a 28-aa peptide derived from pneumococcal surface adhesin A, is a multilineage cell activator in vitro. We hypothesized that P4-mediated activation of phagocytic cells could rapidly and substantially increase opsonophagocytosis of bacteria, which could be translated in vivo to reduced mouse morbidity from fatal pneumococcal infection.

METHODS:

Reference in vitro opsonophagocytic killing and uptake assays were used with suitable effector cells and pathogen-specific antibodies. P4 peptide solution was added at the preopsonization stage. ND4-SW mice were infected intranasally with Streptococcus pneumoniae serotype 3 (WU2). At 72 and 96 h, infected mice received intraperitoneal or intravenous injection of gamma globulin, followed by an injection of P4.

RESULTS:

P4 treatment enhanced in vitro opsonophagocytosis of bacterial pathogens by many fold, and this effect was dependent on complement, P4, and antibody concentrations. Treatment of highly virulent WU2-infected mice with the combination of P4 and serotype-specific antiserum resulted in 100% remission of bacteremia and rescued 80% of the animals (P < .05).

CONCLUSION:

P4 peptide in combination with pathogen-specific antibodies and complement enhances specific opsonophagocytosis and rescues mice from life-threatening pneumococcal infection. P4 peptide provides a fresh direction for therapeutic intervention through augmented passive immunotherapy.

PMID:
19265478
DOI:
10.1086/597425
[Indexed for MEDLINE]

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