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Related Experiment Videos

Group B streptococci inactivate complement component C5a by enzymic cleavage at the C-terminus.

J F Bohnsack1, K W Mollison, A M Buko

  • 1Department of Pediatrics, University of Utah School of Medicine, Salt Lake City 84132.

The Biochemical Journal
|February 1, 1991
PubMed
Summary

Group B Streptococcus (GBS) can inactivate complement component 5a (C5a) by cleaving it near its C-terminus. This GBS activity prevents C5a from activating human immune cells, potentially contributing to GBS infection severity.

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Area of Science:

  • Immunology
  • Microbiology
  • Proteomics

Background:

  • Complement component 5a (C5a) is a crucial mediator in the innate immune response, particularly in neutrophil recruitment and activation.
  • Group B Streptococcus (GBS) is a significant pathogen, especially in neonates, and its mechanisms for evading host defenses are not fully understood.
  • The C-terminal region of C5a is essential for its biological activity, including chemotaxis and adherence of polymorphonuclear leucocytes (PMNs).

Purpose of the Study:

  • To investigate the interaction between GBS and human C5a.
  • To determine the mechanism by which GBS affects C5a function and structure.
  • To explore the potential role of this interaction in GBS pathogenesis.

Main Methods:

  • Incubation of recombinant human C5a (rC5a) with different strains of GBS (7360 and GW).

Related Experiment Videos

  • Assays to measure rC5a's ability to stimulate PMN chemotaxis and adherence.
  • Radioligand binding assays using 125I-labelled rC5a to assess PMN binding.
  • Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) to analyze molecular mass changes.
  • Plasma-desorption mass spectrometry (PDMS) to identify the cleavage site on rC5a.

    • Main Results:

    • GBS strain 7360 inactivated rC5a, abolishing its ability to induce PMN chemotaxis and adherence.
    • This inactivation correlated with reduced rC5a binding to PMNs and a decrease in molecular mass (approx. 600 Da) by SDS-PAGE.
    • GBS strain GW showed minimal effect on rC5a function, binding, or molecular mass.
    • PDMS revealed that GBS strain 7360 cleaves rC5a between histidine-67 and lysine-68, near the C-terminus.

    Conclusions:

    • GBS possesses a C5a-cleaving proteinase activity that inactivates C5a by proteolytic cleavage at its C-terminus.
    • This mechanism effectively impairs C5a-mediated immune cell activation, representing a novel immune evasion strategy for GBS.
    • The identified C5a-cleaving activity may play a significant role in the pathophysiology of GBS infections.