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Transcriptional profiling of macrophages infected with Fonsecaea monophora

Minglan Shi1,2,3, Jiufeng Sun4, Sha Lu1,3

  • 1Department of Dermatology and Venereology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.

Mycoses
|January 19, 2019
PubMed

Insights

This study reveals how melanin in Fonsecaea monophora impacts macrophage immune responses during infection. Melanin content influences gene expression and the MAPK signaling pathway, offering insights into chromoblastomycosis pathogenesis.

Area of Science:

  • Mycology
  • Immunology
  • Molecular Biology

Background:

  • Fonsecaea monophora, a dematiaceous fungus, causes chromoblastomycosis via traumatic inoculation.
  • The early host-pathogen interactions and pathogenesis of F. monophora remain poorly understood.
  • Understanding macrophage responses is crucial for deciphering fungal infection mechanisms.

Purpose of the Study:

  • To investigate the mechanisms by which macrophages combat F. monophora.
  • To elucidate the specific role of fungal melanin in the host-pathogen interaction.
  • To explore how melanin affects macrophage transcriptional profiles and signaling pathways.

Main Methods:

  • RNA sequencing (Illumina platform) was employed to analyze macrophage gene expression.
  • F. monophora strains with varying melanin content were used to challenge macrophages.
  • Functional enrichment analyses were performed on differentially expressed genes.

Main Results:

  • Different melanin levels in F. monophora strains induced distinct macrophage transcriptional profiles.
  • Differentially expressed genes were primarily associated with immune response pathways.
  • Fungal melanin appears to modulate macrophage interactions by regulating the MAPK signaling pathway.

Conclusions:

  • Fungal melanin plays a significant role in the pathogenesis of F. monophora infections.
  • Melanin influences macrophage immune responses, potentially through the MAPK signaling pathway.
  • This research provides novel insights into the molecular mechanisms underlying chromoblastomycosis.

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