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Type I Interferon Response Dysregulates Host Iron Homeostasis and Enhances Candida glabrata Infection.

Abstract：

:Type I interferons (IFNs-I) fulfil multiple protective functions during pathogenic infections, but they can also cause detrimental effects and enhance immunopathology. 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. 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. This leads to enhanced iron accumulation in the phagolysosome and failure to restrict fungal access to iron pools. As a result, C. glabrata acquires iron via the Sit1/Ftr1 iron transporter system, facilitating fungal intracellular replication and immune evasion. 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.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Riedelberger M,Penninger P,Tscherner M,Seifert M,Jenull S,Brunnhofer C,Scheidl B,Tsymala I,Bourgeois C,Petryshyn A,Glaser W,Limbeck A,Strobl B,Weiss G,Kuchler K

doi

10.1016/j.chom.2020.01.023

subject

Has Abstract

pub_date

2020-03-11 00:00:00

pages

454-466.e8

issue

3

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(20)30064-0

journal_volume

27

pub_type

杂志文章

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