Macrophage internalization creates a multidrug-tolerant fungal persister reservoir and facilitates the emergence of drug resistance
Open accessAbstract
Candida glabrata is a major fungal pathogen notable for causing recalcitrant infections, rapid emergence of drug-resistant strains, and its ability to survive and proliferate within macrophages. Resembling bacterial persisters, a subset of genetically drug-susceptible C. glabrata cells can survive lethal exposure to the fungicidal echinocandin drugs. Herein, we show that macrophage internalization induces cidal drug tolerance in C. glabrata, expanding the persister reservoir from which echinocandin-resistant mutants emerge. We show that this drug tolerance is associated with non-proliferation and is triggered by macrophage-induced oxidative stress, and that deletion of genes involved in reactive oxygen species detoxification significantly increases the emergence of echinocandin-resistant mutants. Finally, we show that the fungicidal drug amphotericin B can kill intracellular C. glabrata echinocandin persisters, reducing emergence of resistance. Our study supports the hypothesis that intra-macrophage C. glabrata is a reservoir of recalcitrant/drug-resistant infections, and that drug alternating strategies can be developed to eliminate this reservoir.
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N. glabratus persisters are recalcitrant to echinocandins and AmB.
“N. glabratus persisters are recalcitrant to echinocandins and AmB [38].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [38]
The Results section reports that intracellular C. glabrata persisters are highly tolerant to echinocandins, supporting that part of the claim. But the section titled “Micafungin-tolerant ICG are effectively killed by amphotericin B” reports the opposite for AmB: following micafungin with amphotericin B significantly reduced persister numbers. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredEchinocandins' cidality requires actively growing cells producing a cell wall, whereas amphotericin B indistinguishably kills growing and non-growing cells.
“echinocandins’ cidality requires actively growing cells producing a cell wall, whereas amphotericin B indistinguishably kills growing and non-growing cells (36).”
From Overlooked <i>Candida glabrata</i> petites are echinocandin tolerant, induce host inflammatory responses, and display poor <i>in vivo</i> fitness (2023) · cites this paper as [36]
The Discussion says echinocandin killing may be more dependent on growth because its target is needed for cell-wall building, while amphotericin B can act on growing and non-growing cells. The Results likewise find amphotericin B killing much less dependent on nutrient availability. These passages support the contrast, but not the categorical claims that echinocandins require growth or that amphotericin B kills the two states indistinguishably. (LLM, conf=0.87)
Experimental — accuracy not yet measuredDespite initial susceptibility to drug, heteroresistant subpopulations can expand during therapy, partially due to antifungal exposure, characterized as emergence of resistance-related genetic mutations, and clinically as relapse or progression of infection.
“Despite initial susceptibility to the drug, heteroresistant subpopulations can expand during therapy, partially due to antifungal exposure, characterized as the emergence of resistance-related genetic mutations, and clinically as relapse or progression of the infection [110,151,152,153].”
From Insight into the Mechanisms and Clinical Relevance of Antifungal Heteroresistance (2025) · cites this paper as [110]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredEchinocandin resistance predominantly emerges under specific drug selection pressure, as evidenced by its strong association with prior echinocandin exposure.
“Clinically, echinocandin resistance predominantly emerges under specific drug selection pressure, as evidenced by their strong association with prior echinocandin exposure [44, 45, 46].”
From Calcineurin‐Dependent Stress Adaptation Enables Caspofungin Heteroresistance Leading to Stable Resistance in <i>Candida Glabrata</i> (2026) · cites this paper as [46]
The Introduction (page not provided) reports that increased clinical use of echinocandins was accompanied by more resistant C. glabrata isolates, and that resistant isolates can emerge during infection. The paper does not establish that resistance predominantly arises under drug selection pressure or show a strong patient-level association with prior echinocandin exposure. (LLM, conf=0.86)
Experimental — accuracy not yet measuredCaspofungin stress itself can induce reactive oxygen species (ROS) accumulation, which has been linked to decreased susceptibility and may act as a driver of lipid peroxidation.
“caspofungin stress itself can induce reactive oxygen species (ROS) accumulation [54], which has been linked to decreased susceptibility and may act as a driver of lipid peroxidation”
From Calcineurin‐Dependent Stress Adaptation Enables Caspofungin Heteroresistance Leading to Stable Resistance in <i>Candida Glabrata</i> (2026) · cites this paper as [46]
The Discussion reports that echinocandin treatment increased ROS in C. glabrata, supporting the general point, but it does not establish that caspofungin specifically caused the increase. The paper links ROS to greater tolerance of micafungin; it also says the authors found no evidence of ROS-based damage to lipids, so it does not support the proposed lipid-peroxidation link. Our copy provides no page numbers for these passages. (LLM, conf=0.85)
Experimental — accuracy not yet measured
The similar killing rate is at least partly due to the observed lack of growth dependence of amphotericin B compared to echinocandins.
“This similar killing rate is at least partly due to the observed lack of growth dependence of amphotericin B compared to echinocandins (36).”
From Overlooked <i>Candida glabrata</i> petites are echinocandin tolerant, induce host inflammatory responses, and display poor <i>in vivo</i> fitness (2023) · cites this paper as [36]
Parental strains showed the hallmark of echinocandin persisters.
“The parental strains, however, showed the hallmark of echinocandin persisters, as described previously (36).”
From Overlooked <i>Candida glabrata</i> petites are echinocandin tolerant, induce host inflammatory responses, and display poor <i>in vivo</i> fitness (2023) · cites this paper as [36]
After engulfment into phagosomes by macrophages, C. glabrata cells typically remain viable and survive longer when exposed to echinocandins, resulting in an increased number of long-lived cells.
“After engulfment into phagosomes by macrophages, C. glabrata cells typically remain viable and survive longer when exposed to echinocandins, resulting in an increased number of long-lived cells (31).”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [31]
Tolerance to amphotericin B was also observed for engulfed C. glabrata cells.
“Tolerance to amphotericin B was also observed for engulfed C. glabrata cells (31).”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [31]
Engulfment of C. glabrata cells into phagosomes of macrophages produced elevated micafungin tolerance and persistence.
“Engulfment of C. glabrata cells into phagosomes of macrophages produced elevated micafungin tolerance and persistence (31).”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [31]
Reports on echinocandin-associated persistence primarily focus on intracellular Nakaseomyces glabratus internalized by macrophages.
“Reports on echinocandin-associated persistence are primarily focused on intracellular Nakaseomyces glabratus (also called Candida glabrata), which internalized by macrophage [38,39].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [38]
The phagocytic intracellular environment induces the formation of persisters.
“Studies on pathogen–phagocyte interactions have revealed the inducing effect of the phagocytic intracellular environment on the formation of persisters [110].”
From Insight into the Mechanisms and Clinical Relevance of Antifungal Heteroresistance (2025) · cites this paper as [110]
Persistence, a non-stable resistance phenotype, serves as a reservoir for the evolution of echinocandin resistance.
“Another non‐stable resistance phenotype, persistence, has been demonstrated to serve as a reservoir for the evolution of echinocandin resistance [46].”
From Calcineurin‐Dependent Stress Adaptation Enables Caspofungin Heteroresistance Leading to Stable Resistance in <i>Candida Glabrata</i> (2026) · cites this paper as [46]
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Chen, L., Zhang, L., Xie, Y., Wang, Y., Tian, X., Fang, W., Xue, X., & Wang, L. (2023) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2023.115007 · Cited by 63 · see citing works
Fungicide-tolerant persister formation during cryptococcal pulmonary infection
Ke, W., Xie, Y., Chen, Y., Ding, H., Ye, L., Qiu, H., Li, H., Zhang, L., Chen, L., Tian, X., et al. (2024) · Cell Host & Microbe · doi:10.1016/j.chom.2023.12.012 · Cited by 45 · see citing works
Self-citationArastehfar, A., Daneshnia, F., Hovhannisyan, H., Fuentes, D., Cabrera, N., Quinteros, C., Ilkit, M., Ünal, N., Hilmioğlu-Polat, S., Jabeen, K., et al. (2023) · mBio · doi:10.1128/mbio.01180-23 · Cited by 27 · see citing works
“This similar killing rate is at least partly due to the observed lack of growth dependence of amphotericin B compared to echinocandins (36).”
BackgroundInfluentialSelf-citationArastehfar, A., Daneshnia, F., Floyd, D. J., Jeffries, N. E., Salehi, M., Perlin, D. S., Ilkit, M., Lass-Flöerl, C., & Mansour, M. K. (2024) · mBio · doi:10.1128/mbio.00072-24 · Cited by 19 · see citing works
Self-citationInsight into the Mechanisms and Clinical Relevance of Antifungal Heteroresistance
Su, Y., Li, Y., Yi, Q., Xu, Y., Sun, T., & Li, Y. (2025) · Journal of Fungi · doi:10.3390/jof11020143 · Cited by 18 · see citing works
“Despite initial susceptibility to the drug, heteroresistant subpopulations can expand during therapy, partially due to antifungal exposure, characterized as the emergence of resistance-related genetic mutations, and clinically as relapse or progression of the infection [110,151–153].”
InfluentialAntifungal persistence: Clinical relevance and mechanisms
Wang, R., Lv, J., Chen, L., Zhao, Y., & Du, H. (2025) · PLoS pathogens · doi:10.1371/journal.ppat.1013456 · Cited by 12 · see citing works
Nickels, T. J., & Cunningham, K. W. (2025) · mSphere · doi:10.1128/msphere.00270-25 · Cited by 8 · see citing works
Gonzalez-Jimenez, I., Keniya, M. V., Aptekmann, A. A., Quinteros, C., Wilkerson, A., Arastehfar, A., Daneshnia, F., Perlin, D. S., & Shor, E. (2025) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.00500-25 · Cited by 4 · see citing works
Self-citationHarrington, A. A., Nickels, T. J., & Cunningham, K. W. (2026) · mBio · doi:10.1128/mbio.02546-25 · Cited by 4 · see citing works
Su, Y., Li, Y., Xiao, M., Guo, D., Perlin, D. S., Shor, E., Xu, Y., & Li, Y. (2026) · Advanced Science · doi:10.1002/advs.76369 · Cited by 2 · see citing works
Self-citation
- Authors
- Arastehfar, A., Daneshnia, F., Cabrera, N., Penalva-Lopez, S., Sarathy, J., Zimmerman, M., Shor, E., & Perlin, D. S.
- Affiliations
- Hackensack Meridian Health (US)
- Corresponding author
- Shor, Erika
- Perlin, David S.
- Venue
- Nature Communications
- Published
- 2023-03-02
- Volume
- 14
- Issue
- 1
- Pages
- 1183-1183
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9981703
- OpenAlex
- W4322760718
- Cited by
- 58
- References
- 70
- Citations by year
- 2026: 13 · 2025: 23 · 2024: 13 · 2023: 9
- FWCI
- 11.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (5R01AI109025)
- 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 glabrata, macrophage uptake, echinocandin resistance, drug tolerance, oxidative stress, reactive oxygen species scavenging, amphotericin B, antifungal resistance, drug combination therapy
- MeSH terms
- Antifungal Agents, Drug Resistance, Drug Tolerance, Macrophages, Candida glabrata, Echinocandins
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