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Cited by 29Antifungal resistance and susceptibilityFungal and yeast genetics researchFungal Infections and Studies

Candida auris —macrophage cellular interactions and transcriptional response

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Miramón, Pedro, Pountain, Andrew W., Lorenz, Michael C.·2023·Infection and Immunity
DOI 10.1128/iai.00274-23PMC PMC10652981
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Abstract

The pathogenic yeast Candida auris represents a global threat of the utmost clinical relevance. This emerging fungal species is remarkable in its resistance to commonly used antifungal agents and its persistence in the nosocomial settings. The innate immune system is one the first lines of defense preventing the dissemination of pathogens in the host. C. auris is susceptible to circulating phagocytes, and understanding the molecular details of these interactions may suggest routes to improved therapies. In this work, we examined the interactions of this yeast with macrophages. We found that macrophages avidly phagocytose C. auris ; however, intracellular replication is not inhibited, indicating that C. auris resists the killing mechanisms imposed by the phagocyte. Unlike Candida albicans , phagocytosis of C. auris does not induce macrophage lysis. The transcriptional response of C. auris to macrophage phagocytosis is very similar to other members of the CUG clade ( C. albicans, C. tropicalis, C. parapsilosis, C. lusitaniae ), i.e., downregulation of transcription/translation and upregulation of alternative carbon metabolism pathways, transporters, and induction of oxidative stress response and proteolysis. Gene family expansions are common in this yeast, and we found that many of these genes are induced in response to macrophage co-incubation. Among these, amino acid and oligopeptide transporters, as well as lipases and proteases, are upregulated. Thus, C. auris shares key transcriptional signatures shared with other fungal pathogens and capitalizes on the expansion of gene families coding for potential virulence attributes that allow its survival, persistence, and evasion of the innate immune system.

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  • C. albicans employs β-oxidation (POX1, FOX2, POT1), the glyoxylate cycle (ICL1, MLS1), and gluconeogenesis to generate glucose from fatty acids for growth.

    “For example, C. albicans employs β-oxidation ( POX1 , FOX2 , POT1 ), the glyoxylate cycle ( ICL1 , MLS1 ), and gluconeogenesis to generate glucose from fatty acids for growth (31-36).”

    From <i>Candida auris</i> metabolism and growth preferences in physiologically relevant skin-like conditions (2026) · cites this paper as [34]

    The Discussion says that C. albicans switches to using fatty acids and that this metabolic adaptation is critical for survival. The paper does not specify the claimed POX1/FOX2/POT1 and ICL1/MLS1 pathways or say that they generate glucose from fatty acids for growth; its mention of ICL1 and FOX2 concerns the C. auris transcriptional response. (LLM, conf=0.85)

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  • Both conventional and alternative carbon metabolism allow C. albicans to grow in various nutrient sources.

    “Taken together, both conventional and alternative carbon metabolism allow C. albicans to grow in various nutrient sources.”

    From <i>Candida auris</i> metabolism and growth preferences in physiologically relevant skin-like conditions (2026) · cites this paper as [34]

    The Discussion (page unavailable) says C. albicans switches to using organic, fatty, and amino acids and that this adaptation is critical for survival within macrophages. This supports the alternative-carbon-metabolism part, but the paper does not establish that conventional and alternative metabolism together allow C. albicans to grow across various nutrient sources. (LLM, conf=0.85)

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Cited by

Sorted by citations

Authors
Miramón, P., Pountain, A. W., & Lorenz, M. C.
Affiliations
  • The University of Texas Health Science Center at Houston (US)
  • NYU Langone Health (US)
ORCID
Venue
Infection and Immunity
Publisher
American Society for Microbiology
Published
2023-11-16
Volume
91
Issue
11
Pages
e0027423-e0027423
ISSN
  • 0019-9567 (ISSN-L)
  • 1098-5522
DOI
10.1128/iai.00274-23
PMC
PMC10652981
OpenAlex
W4387472260
Cited by
29
References
15
Citations by year
2026: 13 · 2025: 7 · 2024: 9
FWCI
6.00
Type
journal article
Language
en
Open access
Licence
Locations
  • Infection and Immunity (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Digital Commons-TMC (Texas Medical Center) (submittedVersion)
Funders
HHS | National Institutes of Health (R01AI143304)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
Keywords
Candida auris, macrophage phagocytosis, innate immune evasion, transcriptional response, oxidative stress response, proteolysis, gene family expansion, antifungal resistance, nosocomial fungal infections, Candida albicans
MeSH terms
Candida parapsilosis, Candida auris, Antifungal Agents, Candida, Candida albicans, Macrophages

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