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Related Experiment Videos

Experimental pulmonary candidiasis.

R T Sawyer1

  • 1Trudeau Institute, Saranac Lake, NY 12983.

Mycopathologia
|February 1, 1990
PubMed
Summary

Pulmonary tissue is highly resistant to Candida albicans infection due to resident pulmonary alveolar macrophages (PAM) that rapidly kill the yeast. This potent antifungal activity is linked to changes in macrophage surface molecules.

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Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Candida albicans is an opportunistic fungal pathogen.
  • Pulmonary infections can arise from various routes of exposure.
  • The host immune response in the lungs is critical for controlling fungal burden.

Purpose of the Study:

  • To investigate the initial interaction between Candida albicans and mouse pulmonary tissue.
  • To determine the role of pulmonary alveolar macrophages (PAM) in controlling C. albicans infection.
  • To explore strain-specific differences in macrophage antifungal activity.

Main Methods:

  • Intravenous (IV) and intratracheal (IT) challenge models in B6D2/F1 mice.
  • In vitro killing assays using resident PAM against C. albicans.
  • Flow cytometry to analyze surface molecule expression (F4/80, Mac 1) on PAM.
  • Assessment of C. albicans growth and dissemination in murine lungs.

Main Results:

  • The LD50 for IV challenge was significantly lower than for IT challenge, indicating pulmonary resistance.
  • Resident PAM effectively killed C. albicans in vitro, inhibiting yeast proliferation and germ tube formation.
  • Antifungal activity was associated with resident PAM from mice with a black 6 background.
  • In vivo, PAM showed downregulated F4/80 and upregulated Mac 1 expression during early infection.

Conclusions:

  • Murine pulmonary tissue exhibits significant resistance to C. albicans, primarily mediated by resident PAM.
  • PAM's ability to phagocytize and kill C. albicans is a key factor in controlling pulmonary infection.
  • Macrophage surface molecule expression (F4/80, Mac 1) is altered during C. albicans interaction, suggesting modulation of immune function.

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