ArticlePloS one2011
Polyene macrolide antifungal drugs trigger interleukin-1β secretion by activating the NLRP3 inflammasome.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Conventional amphotericin B elicits markers of immunogenic cell death on leukemic blasts, mediates immunostimulatory effects on phagocytic cells, and synergizes with PD-L1 blockade.Oncoimmunology · 2022Article
- Gefitinib initiates sterile inflammation by promoting IL-1β and HMGB1 release via two distinct mechanisms.Cell death & disease · 2021Article
- The Role of Signaling via Aqueous Pore Formation in Resistance Responses to Amphotericin B.Antimicrobial agents and chemotherapy · 2016Review
- Biotechnological production and application of the antibiotic pimaricin: biosynthesis and its regulation.Applied microbiology and biotechnology · 2016Review
- Candida albicans Targets a Lipid Raft/Dectin-1 Platform to Enter Human Monocytes and Induce Antigen Specific T Cell Responses.PloS one · 2015Article
- Review
- Adenosine-5'-triphosphate (ATP) protects mice against bacterial infection by activation of the NLRP3 inflammasome.PloS one · 2013Article
- Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1β secretion.The Journal of clinical investigation · 2013Article
- Uromodulin triggers IL-1β-dependent innate immunity via the NLRP3 inflammasome.Journal of the American Society of Nephrology : JASN · 2012Article
- Experimental central nervous system aspergillosis therapy: efficacy, drug levels and localization, immunohistopathology, and toxicity.Antimicrobial agents and chemotherapy · 2012Article
- Suppression of ribosomal function triggers innate immune signaling through activation of the NLRP3 inflammasome.PloS one · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The use of antimycotic drugs in fungal infections is based on the concept that they suppress fungal growth by a direct killing effect. However, amphotericin and nystatin have been reported to also trigger interleukin-1β (IL-1β) secretion in monocytes but the molecular mechanism is unknown. Here we report that only the polyene macrolides amphotericin B, nystatin, and natamycin but none of the tested azole antimycotic drugs induce significant IL-1β secretion in-vitro in dendritic cells isolated from C57BL/6 mouse bone marrow. IL-1β release depended on Toll-like receptor-mediated induction of pro-IL-1β as well as the NLRP3 inflammasome, its adaptor ASC, and caspase-1 for enzymatic cleavage of pro-IL-1β into its mature form. All three drugs induced potassium efflux from the cells as a known mechanism for NLRP3 activation but the P2X7 receptor was not required for this process. Natamycin-induced IL-1β secretion also involved phagocytosis, as cathepsin activation as described for crystal-induced IL-1β release. Together, the polyene macrolides amphotericin B, nystatin, and natamycin trigger IL-1β secretion by causing potassium efflux from which activates the NLRP3-ASC-caspase-1. We conclude that beyond their effects on fungal growth, these antifungal drugs directly activate the host's innate immunity.
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