Dietary restriction of iron availability attenuates UPEC pathogenesis in a mouse model of urinary tract infection.
Bauckman KA1, Matsuda R2, Higgins CB3, DeBosch BJ3, Wang C4, Mysorekar IU5.
Am J Physiol Renal Physiol. 2019 Feb 6. doi: 10.1152/ajprenal.00133.2018. Abstract
Iron is a critical nutrient required by hosts and pathogens. Uropathogenic Escherichia coli (UPEC), the principal causative agent of urinary tract infections (UTIs), chelate iron for their survival and persistence. Here, we demonstrate that dietary
modulation of iron availability limits UPEC burden in a mouse model of UTI. Mice on a low iron diet exhibit reduced systemic and bladder mucosal iron availability, harbor significantly lower bacterial burden, concomitant with dampened inflammation.
Hepcidin is a master regulator of iron that controls iron-dependent UPEC intracellular growth. Hepcidin deficient mice ( Hamp1-/- ) exhibit accumulation of iron deposits, persistent bacterial burden in the bladder, and a heightened inflammatory response
to UTI. However, a low iron dietary regimen reverses the iron overload and increased bacterial burden phenotypes in Hamp1-/- mice. Thus, modulation of iron levels via diet can reduce UPEC infection and persistence, which may have significant implications
for clinical management of UTI.

KEYWORDS:
Ferritin; IL-6; hepcidin; uropathogenic E. coli; urothelium

PMID: 30724105 DOI: 10.1152/ajprenal.00133.2018

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