Integrity under stress: Host membrane remodelling and damage by fungal pathogens

Johannes Westman, Bernhard Hube, Gregory D. Fairn

Research output: Contribution to journalReview articlepeer-review

28 Citations (Scopus)

Abstract

Membrane bilayers of eukaryotic cells are an amalgam of lipids and proteins that distinguish organelles and compartmentalise cellular functions. The mammalian cell has evolved mechanisms to sense membrane tension or damage and respond as needed. In the case of the plasma membrane and phagosomal membrane, these bilayers act as a barrier to microorganisms and are a conduit by which the host interacts with pathogens, including fungi such as Candida, Cryptococcus, Aspergillus, or Histoplasma species. Due to their size, morphological flexibility, ability to produce long filaments, secrete pathogenicity factors, and their potential to replicate within the phagosome, fungi can assault host membranes in a variety of physical and biochemical ways. In addition, the recent discovery of a fungal pore-forming peptide toxin further highlights the importance of membrane biology in the outcomes between host and fungal cells. In this review, we discuss the apparent “stretching” of membranes as a sophisticated biological response and the role of vesicular transport in combating membrane stress and damage. We also review the known pathogenicity factors and physical properties of fungal pathogens in the context of host membranes and discuss how this may contribute to pathogenic interactions between fungal and host cells.

Original languageEnglish
Article numbere13016
JournalCellular Microbiology
Volume21
Issue number4
DOIs
Publication statusPublished - Apr 2019
Externally publishedYes

Bibliographical note

Funding Information:
Research involving macrophage cell biology in GDF's lab is funded by the Canadian Institute of Health Research and the JP Bickell Foundation. J.W. is supported by EMBO Long‐Term Fellowship (ALTF 18‐2016), and BH is supported by the Deutsche Forschungsgemeinschaft CRC/TR FungiNet Project C1, the Leibniz Association Campus InfectoOptics SAS‐2015‐HKI‐LWC, the Infect ERA‐NET Program FunComPath (BMBF 031L0001A), and the H2020–Marie Skłodowska‐Curie Actions–European Training Networks–Marie Sklodowska‐Curie (grant agreement no. 642095) —“OPATHY.”

Funding Information:
Canadian Institutes of Health Research, Grant/ Award Number: MOP‐133656; Leibniz Association Campus InfectoOptics, Grant/Award Number: SAS‐2015‐HKI‐LWC; Deutsche Forschungsgemeinschaft CRC/TR FungiNet Project C1; EMBO Long‐Term Fellowship, Grant/Award Number: ALTF 18‐2016; Canadian Institute of Health Research

Funding Information:
Research involving macrophage cell biology in GDF's lab is funded by the Canadian Institute of Health Research and the JP Bickell Foundation. J.W. is supported by EMBO Long-Term Fellowship (ALTF 18-2016), and BH is supported by the Deutsche Forschungsgemeinschaft CRC/TR FungiNet Project C1, the Leibniz Association Campus InfectoOptics SAS-2015-HKI-LWC, the Infect ERA-NET Program FunComPath (BMBF 031L0001A), and the H2020?Marie Sk?odowska-Curie Actions?European Training Networks?Marie Sklodowska-Curie (grant agreement no. 642095)??OPATHY.?

Publisher Copyright:
© 2019 John Wiley & Sons Ltd

ASJC Scopus Subject Areas

  • Microbiology
  • Immunology
  • Virology

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