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Cited by 141Antifungal resistance and susceptibilityGut microbiota and healthImmunodeficiency and Autoimmune Disorders

Long-term antibiotic exposure promotes mortality after systemic fungal infection by driving lymphocyte dysfunction and systemic escape of commensal bacteria

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Drummond, Rebecca A., Desai, Jigar V., Ricotta, Emily E., Swamydas, Muthulekha, Deming, Clay, Conlan, Sean, Quinones, Mariam, Matei-Rascu, Veronika +12 more·2022·Cell Host & Microbe
DOI 10.1016/j.chom.2022.04.013PMC PMC9283303
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Abstract

Antibiotics are a modifiable iatrogenic risk factor for the most common human nosocomial fungal infection, invasive candidiasis, yet the underlying mechanisms remain elusive. We found that antibiotics enhanced the susceptibility to murine invasive candidiasis due to impaired lymphocyte-dependent IL-17A- and GM-CSF-mediated antifungal immunity within the gut. This led to non-inflammatory bacterial escape and systemic bacterial co-infection, which could be ameliorated by IL-17A or GM-CSF immunotherapy. Vancomycin alone similarly enhanced the susceptibility to invasive fungal infection and systemic bacterial co-infection. Mechanistically, vancomycin reduced the frequency of gut Th17 cells associated with impaired proliferation and RORγt expression. Vancomycin's effects on Th17 cells were indirect, manifesting only in vivo in the presence of dysbiosis. In humans, antibiotics were associated with an increased risk of invasive candidiasis and death after invasive candidiasis. Our work highlights the importance of antibiotic stewardship in protecting vulnerable patients from life-threatening infections and provides mechanistic insights into a controllable iatrogenic risk factor for invasive candidiasis.

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  • Vancomycin impairs lymphocyte-dependent IL-17 responses at mucosal barriers.

    “and to impair lymphocyte-dependent IL-17 responses at mucosal barriers [49].”

    From Host–Candida auris interactions in the skin (2026) · cites this paper as [49]

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Authors
Drummond, R. A., Desai, J. V., Ricotta, E. E., Swamydas, M., Deming, C., Conlan, S., Quinones, M., Matei-Rascu, V., Sheriff, L., Lecky, D., Lee, C.-C. R., Green, N. M., Collins, N., Zelazny, A. M., Prevots, D. R., Bending, D., Withers, D., Belkaid, Y., Segre, J. A., & Lionakis, M. S.
Affiliations
  • National Institutes of Health (US)
  • University of Birmingham (GB)
Corresponding author
  • Drummond, Rebecca A.
  • Lionakis, Michail S.
ORCID
Venue
Cell Host & Microbe
Publisher
Elsevier BV
Published
2022-07
Volume
30
Issue
7
Pages
1020-1033.e6
ISSN
1931-3128 (ISSN-L)
DOI
10.1016/j.chom.2022.04.013
PMC
PMC9283303
OpenAlex
W4280601441
Cited by
141
References
15
Citations by year
2026: 24 · 2025: 49 · 2024: 33 · 2023: 26 · 2022: 9
FWCI
14.42
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Host & Microbe (publishedVersion)
  • PubMed (publishedVersion)
  • University of Birmingham Research Portal (University of Birmingham) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (acceptedVersion)
Funders
  • NIH Clinical Center
  • National Human Genome Research Institute
  • NHLBI DIR
  • National Cancer Institute
  • National Institutes of Health
  • National Institute of Allergy and Infectious Diseases
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
Keywords
antibiotic exposure, invasive candidiasis, systemic fungal infection, mortality, lymphocyte dysfunction, Th17 cells, IL-17A, GM-CSF, gut dysbiosis, commensal bacteria, bacterial co-infection, vancomycin, RORγt, antibiotic stewardship, nosocomial infections, immunotherapy
MeSH terms
Animals, Anti-Bacterial Agents, Bacteria, Candida albicans, Candidiasis, Humans, Iatrogenic Disease, Immunotherapy, Vancomycin, Granulocyte-Macrophage Colony-Stimulating Factor, Interleukin-17, Mice, Candidiasis, Invasive, Th17 Cells, Coinfection

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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