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Caspofungin modulates inflammatory responses to Aspergillus fumigatus through stage-specific effects on fungal

T M Hohl1, M Feldmesser, D S Perlin

  • 1Infectious Diseases Service, Memorial Sloan-Kettering Cancer Center and Immunology Program, Sloan-Kettering Institute, New York 10021, USA. hohlt@mskcc.org

The Journal of Infectious Diseases
|May 27, 2008
PubMed

Insights

Echinocandins alter Aspergillus fumigatus morphology, increasing fungal beta-glucan exposure. This enhances Dectin-1-mediated inflammatory responses, impacting treatment strategies for invasive aspergillosis.

Area of Science:

  • Mycology
  • Immunology
  • Pharmacology

Background:

  • Echinocandins are antifungal drugs targeting beta-1,3 glucan synthesis.
  • They are used to treat invasive aspergillosis but do not fully inhibit Aspergillus fumigatus growth.
  • Beta-1,3 glucans are key fungal components that activate host immune responses via Dectin-1.

Purpose of the Study:

  • To investigate the impact of echinocandins on inflammatory responses to Aspergillus fumigatus.
  • To determine if echinocandin-induced morphological changes affect beta-glucan exposure and host immune cell activation.

Main Methods:

  • Treatment of Aspergillus fumigatus conidia and germlings with echinocandins (caspofungin, micafungin).
  • Co-incubation of treated and untreated fungal forms with macrophages.
  • Measurement of inflammatory cytokine secretion (TNF, CXCL2).
  • Assessment of beta-glucan exposure using antibody staining.

Main Results:

  • Echinocandin-treated conidia and germlings showed reduced TNF and CXCL2 secretion by macrophages, correlating with decreased beta-glucan exposure.
  • Echinocandin-treated hyphae induced increased TNF and CXCL2 release from macrophages.
  • Hyphal tips of echinocandin-treated fungi exhibited intense beta-glucan staining.

Conclusions:

  • Echinocandin treatment induces morphological changes in Aspergillus fumigatus hyphae, leading to increased beta-glucan exposure.
  • This increased exposure enhances Dectin-1-mediated inflammatory responses by macrophages.
  • Findings suggest a complex interplay between echinocandins, fungal morphology, and host immunity in aspergillosis treatment.

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