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Related Experiment Videos

Tumor necrosis factor and Candida albicans.

J Y Djeu1

  • 1University of South Florida College of Medicine, Department of Medical Microbiology and Immunology, Tampa 33612.

Behring Institute Mitteilungen
|February 1, 1991
PubMed
Summary

Human large granular lymphocytes (LGL) and neutrophils combat C. albicans through cytokine interactions. Neutrophils release tumor necrosis factor (TNF) when exposed to fungi, enhancing their own antifungal activity.

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Area of Science:

  • Immunology
  • Microbiology

Background:

  • Opportunistic fungal infections, such as those caused by Candida albicans, pose a significant threat to immunocompromised individuals.
  • Effective host defense mechanisms are crucial for controlling fungal growth and preventing disseminated disease.

Purpose of the Study:

  • To investigate the role of cytokines, specifically tumor necrosis factor (TNF), in the interaction between human immune cells and Candida albicans.
  • To elucidate the mechanisms by which neutrophils (PMN) and large granular lymphocytes (LGL) contribute to antifungal defense.

Main Methods:

  • Analysis of cytokine production by LGL and PMN upon exposure to C. albicans.
  • Measurement of TNF using a 51Cr release assay with WEHI 164 tumor cells.
  • Assessment of PMN antifungal activity via a 3H-glucose incorporation assay.

Main Results:

  • LGL rapidly release TNF upon C. albicans exposure, stimulating PMN antifungal activity.
  • C. albicans can also induce TNF production directly from PMN.
  • TNF production by PMN is sensitive to inhibitors of RNA and protein synthesis.
  • Low concentrations of TNF significantly enhance PMN's ability to control C. albicans growth.

Conclusions:

  • TNF production is a normal response of PMN to fungal stimulation.
  • TNF release may contribute to autocrine activation of PMN effector functions against C. albicans.
  • These findings highlight a novel aspect of innate immunity against fungal pathogens.

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