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Beyond tug-of-war: Iron metabolism in cooperative host–microbe interactions
About the Authors: Grischa Y. Chen Affiliation: Molecular and Systems Physiology Lab, Gene Expression Lab, NOMIS Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, California, United States of America Janelle S. Ayres * E-mail: jayres@salk.edu A...
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Published in: | PLoS pathogens 2020-08, Vol.16 (8), p.e1008698-e1008698 |
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Main Authors: | , |
Format: | Article |
Language: | English |
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Online Access: | Get full text |
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Summary: | About the Authors: Grischa Y. Chen Affiliation: Molecular and Systems Physiology Lab, Gene Expression Lab, NOMIS Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, California, United States of America Janelle S. Ayres * E-mail: jayres@salk.edu Affiliation: Molecular and Systems Physiology Lab, Gene Expression Lab, NOMIS Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, California, United States of America ORCID logo http://orcid.org/0000-0002-0809-2494 Introduction Infections induce dramatic rearrangements in host macro- and micronutrient processes [1] and likely reflect host adaptive mechanisms to defend against infection. Alternative functions of microbial siderophores on host physiology Siderophores are molecules that chelate external iron with high affinity and transport iron into microorganisms through dedicated transport systems [10]. [...]siderophores are essential virulence factors for many microbial pathogens [11]. BV, biliverdin; cDC, conventional dendritic cell; CO, carbon monoxide; Ent, enterobactin; FTH, ferritin; glc, glucose; HO-1, heme oxygenase; IR, insulin resistance; RBC, red blood cell. https://doi.org/10.1371/journal.ppat.1008698.g001 Hepcidin in wound repair During acute infections, individuals experience inflammation-dependent hypoferremia [18]. Regulation of iron levels was necessary for proper microbiome composition and mucosal repair because cDC-specific hepcidin-deficient mice were slower to recover following intestinal damage [26]. [...]unlike hepatocyte-derived hepcidin required for systemic infections, cDC-derived hepcidin promotes intestinal homeostasis. |
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ISSN: | 1553-7374 1553-7366 1553-7374 |
DOI: | 10.1371/journal.ppat.1008698 |