The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages

Lim, Daejin and Kim, Kwang Soo and Jeong, Jae-Ho and Marques, Oriana and Kim, Hyun-Ju and Song, Miryoung and Lee, Tae-Hoon and Kim, Jae Il and Choi, Hueng-Sik and Min, Jung-Joon and Bumann, Dirk and Muckenthaler, Martina U. and Choy, Hyon E.. (2018) The hepcidin-ferroportin axis controls the iron content of Salmonella-containing vacuoles in macrophages. Nature communications, 9 (1). p. 2091.

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Macrophages release iron into the bloodstream via a membrane-bound iron export protein, ferroportin (FPN). The hepatic iron-regulatory hormone hepcidin controls FPN internalization and degradation in response to bacterial infection. Salmonella typhimurium can invade macrophages and proliferate in the Salmonella-containing vacuole (SCV). Hepcidin is reported to increase the mortality of Salmonella-infected animals by increasing the bacterial load in macrophages. Here we assess the iron levels and find that hepcidin increases iron content in the cytosol but decreases it in the SCV through FPN on the SCV membrane. Loss-of-FPN from the SCV via the action of hepcidin impairs the generation of bactericidal reactive oxygen species (ROS) as the iron content decreases. We conclude that FPN is required to provide sufficient iron to the SCV, where iron serves as a cofactor for the generation of antimicrobial ROS rather than as a nutrient for Salmonella.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Infection Biology > Molecular Microbiology (Bumann)
UniBasel Contributors:Bumann, Dirk
Item Type:Article, refereed
Article Subtype:Research Article
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:27 Apr 2020 18:12
Deposited On:27 Apr 2020 18:12

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