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Macrophage-independent fungicidal action of the pulmonary collectins

Francis X McCormack1, Reta Gibbons, Susan R Ward

  • 1Veterans Affairs Medical Center, Cincinnati, Ohio 45220, USA. frank.mccormack@uc.edu

The Journal of Biological Chemistry
|July 15, 2003
PubMed

Insights

Pulmonary surfactant proteins A and D (SP-A, SP-D) directly kill Histoplasma capsulatum yeast by increasing its permeability. However, Histoplasma capsulatum evades this killing by entering lung macrophages.

Area of Science:

  • Pulmonary immunology
  • Mycology
  • Infectious diseases

Background:

  • Histoplasma capsulatum (Hc) is a fungal pathogen causing pneumonia.
  • Pulmonary collectins, surfactant proteins (SP) A and D, are key innate immune molecules in the lung.

Purpose of the Study:

  • To investigate the role of SP-A and SP-D in clearing Hc yeast from the lungs.
  • To determine the direct effects of SP-A and SP-D on Hc viability and permeability.

Main Methods:

  • In vitro exposure of Hc yeast to SP-A and SP-D.
  • Measurement of Hc growth and viability.
  • Assessment of yeast cell permeability.
  • In vivo studies using SP-A null mice.

Main Results:

  • SP-A and SP-D exposure decreased Hc viability and growth, indicating yeast killing.
  • Collectins increased Hc cell permeability, leading to leakage and enzyme activity.
  • SP-A null mice showed modest susceptibility to Hc infection, with fewer CD8+ cells in lungs.
  • SP-A and SP-D did not inhibit Hc growth within macrophages.

Conclusions:

  • SP-A and SP-D exhibit direct antimicrobial activity against Hc by disrupting cell permeability.
  • Hc evades collectin-mediated killing by rapidly internalizing into pulmonary macrophages.

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