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Modulation of Urinary Siderophores by the Diet, Gut Microbiota and Inflammation in Mice
Author(s) -
Xiao Xia,
Yeoh Beng San,
Saha Piu,
Tian Yuan,
Singh Vishal,
Patterson Andrew D.,
VijayKumar Matam
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.315.5
Subject(s) - siderophore , urinary system , urine , inflammation , biology , gut flora , microbiology and biotechnology , bacteria , endocrinology , immunology , genetics
Mammalian siderophores are believed to play a critical role in maintaining iron homeostasis. However, the properties and functions of mammalian siderophores have not been fully clarified. In this study, we have employed Chrome Azurol S (CAS) assay which is a well‐established method for bacterial siderophores study, to detect and quantify mammalian siderophores in urine samples. Our study demonstrates that siderophores in urine can be altered by diet, gut microbiota, and inflammation. C57BL/6 mice, fed on plant‐based chow diets which contain numerous phytochemicals, have more siderophores in the urine compared to those fed on purified diets. Urinary siderophores were upregulated in iron overload conditions, but not altered by other tested nutrients status. Further, germ‐free mice displayed 50% reduced urinary siderophores, in comparison to conventional mice, indicating microbiota biotransformation is critical in generating or stimulating host metabolism to create more siderophores. Altered urinary siderophores levels during inflammation suggest that host health conditions influence systemic siderophores level. This is the first report to measure urinary siderophores as a whole, describing how siderophores levels are modulated under different physiological conditions. We believe that our study opens up a new field in mammalian siderophores research and the technique we used in a novel manner has the potential to be applied to clinical purpose. Support or Funding Information This work was supported by grants from the National Institutes of Health (NIH) R01 [Grant number DK097865].