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Measuring Phagocytosis of Aspergillus fumigatus Conidia by Human Leukocytes using Flow Cytometry
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Measuring Phagocytosis of Aspergillus fumigatus Conidia by Human Leukocytes using Flow Cytometry

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Aspergillus conidia activate the complement by the mannan-binding lectin C2 bypass mechanism

Chantal Dumestre-Pérard1, Bertrand Lamy, Delphine Aldebert

  • 1Laboratoire Adaptation et Pathogénie des Micro-organismes, Université Joseph Fourier, Grenoble 1, BP 170, Grenoble, France. Chantal.Dumestre@ujf-grenoble.fr

Journal of Immunology (Baltimore, Md. : 1950)
|November 5, 2008
PubMed

Insights

Mannan-binding lectin (MBL) directly supports complement C3 activation via a C2 bypass mechanism, enhancing innate immunity against Aspergillus fungal infections. This finding is crucial for understanding host defense in invasive aspergillosis.

Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Innate immunity is critical for defense against invasive aspergillosis.
  • Mannan-binding lectin (MBL) is a key component of the innate immune system.
  • The role of MBL in complement activation against Aspergillus remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of MBL in complement activation against Aspergillus conidia.
  • To determine if MBL can initiate complement pathways against fungal infections.
  • To compare complement activation by clinical and environmental Aspergillus strains.

Main Methods:

  • In vitro studies using 29 Aspergillus conidia strains from five species.
  • Incubation with human normal serum and MBL-deficient serum.
  • Reconstitution experiments with MBL/MASPs complexes.
  • Analysis of complement activation pathways (classical, lectin, alternative).

Main Results:

  • Aspergillus conidia activated the alternative complement pathway but not classical or lectin pathways.
  • MBL directly supports C3 activation through a C2 bypass mechanism.
  • Clinical Aspergillus strains showed stronger alternative pathway activation than environmental strains.

Conclusions:

  • MBL plays a direct role in complement activation against Aspergillus via a C2 bypass mechanism.
  • This MBL-mediated complement activation contributes to innate immunity against invasive aspergillosis.
  • Clinical Aspergillus isolates exhibit enhanced complement activation, suggesting potential virulence factors.

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