Thus, IFNs-I are central regulators of iron homeostasis, which can impact infection, and restricting iron bioavailability may offer therapeutic strategies to combat invasive fungal infections. As a result, C. glabrata acquires iron via the Sit1/Ftr1 iron transporter system, facilitating fungal intracellular replication and immune evasion. This leads to enhanced iron accumulation in the phagolysosome and failure to restrict fungal access to iron pools. grade, Emsure) and 100 L of hydrogen peroxide (30. Total Metal Quantification by ICP-MS 50 L BMDM lysates were digested in closed PFA vials with 200 L nitric acid (65, p.a. By engaging JAK1, IFNs-I disturb the balance of the transcriptional activator NRF2 and repressor BACH1 to induce downregulation of the key iron exporter Fpn1 in macrophages. The MFI(DHE) (median fluorescence intensity) of BMDMs was collected on a LSRFortessa (BD Biosciences) and analyzed using FlowJo software version 7.6.5 (FlowJo). Here, we report that IFNs-I promote the dysregulation of iron homeostasis in macrophages during systemic infections with the intracellular pathogen Candida glabrata, leading to fungal survival and persistence. ![]() Type I interferons (IFNs-I) fulfil multiple protective functions during pathogenic infections, but they can also cause detrimental effects and enhance immunopathology.
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