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Related Experiment Videos

Activation, binding, and processing of complement component 3 (C3) by Blastomyces dermatitidis

M X Zhang1, B Klein

  • 1Department of Pediatrics, Comprehensive Cancer Center, University of Wisconsin Medical School, University of Wisconsin Hospital and Clinics, Madison 53792, USA.

Infection and Immunity
|May 1, 1997
PubMed
Summary
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Blastomyces dermatitidis activates complement's C3 via both classical and alternative pathways, primarily through its beta-glucan. This interaction facilitates phagocyte recognition and killing of the yeast.

Area of Science:

  • Immunology
  • Mycology
  • Microbial Pathogenesis

Background:

  • Complement system activation is crucial for host defense against fungal pathogens like Blastomyces dermatitidis.
  • Understanding how complement components, particularly C3, interact with B. dermatitidis is essential for elucidating host-pathogen dynamics.

Purpose of the Study:

  • To characterize the activation, binding, and processing of C3 by B. dermatitidis.
  • To investigate the roles of classical and alternative complement pathways in C3 deposition on B. dermatitidis.
  • To identify the fungal components involved in initiating complement activation.

Main Methods:

  • Utilized pooled normal human serum (NHS) with and without MgEGTA to assess complement pathway activation.
  • Quantified C3 deposition on yeast cells using flow cytometry.

Related Experiment Videos

  • Investigated the role of immunoglobulins and beta-glucan in complement activation.
  • Analyzed C3 processing products (C3b, iC3b) using hydroxylamine treatment.

    • Main Results:

    • B. dermatitidis activates C3 via both classical and alternative pathways, with significant intrinsic alternative pathway activation.
    • Yeast cell wall beta-glucan is a target for initiating antibodies in the classical pathway.
    • C3 deposition occurs rapidly, with C3b and iC3b predominantly bound via ester linkages to yeast polysaccharides.
    • Rapid conversion of C3b to iC3b suggests a specific opsonization state.

    Conclusions:

    • B. dermatitidis efficiently activates complement C3 through both pathways, with the alternative pathway being intrinsically active.
    • Antibodies targeting beta-glucan initiate the classical pathway, leading to robust C3 deposition.
    • The resulting C3b and iC3b opsonization likely mediates phagocyte recognition via CR1 and CR3 receptors, influencing fungal clearance.