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- W1945885800 abstract "The iron-regulatory peptide hepcidin exhibits antimicrobial activity. Having previously shown hepcidin expression in the kidney, we addressed its role in urinary tract infection (UTI), which remains largely unknown. Experimental UTI was induced in wild-type (WT) and hepcidin-knockout (Hepc-/-) mice using the uropathogenic Escherichia coli CFT073 strain. Compared with infected WT mice, infected Hepc-/- mice showed a dramatic increase in renal bacterial load. Moreover, bacterial invasion was significantly dampened by the pretreatment of WT mice with hepcidin. Infected Hepc-/- mice exhibited decreased iron accumulation in the renal medulla and significant attenuation of the renal inflammatory response. Notably, we demonstrated in vitro bacteriostatic activity of hepcidin against CFT073. Furthermore, CFT073 repressed renal hepcidin, both in vivo and in cultured renal cells, and reduced phosphorylation of SMAD kinase in vivo, suggesting a bacterial strategy to escape the antimicrobial activities of hepcidin. In conclusion, we provide new mechanisms by which hepcidin contributes to renal host defense and suggest that targeting hepcidin offers a strategy to prevent bacterial invasion." @default.
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- W1945885800 date "2015-08-20" @default.
- W1945885800 modified "2023-10-14" @default.
- W1945885800 title "Hepcidin as a Major Component of Renal Antibacterial Defenses against UropathogenicEscherichia coli" @default.
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- W1945885800 doi "https://doi.org/10.1681/asn.2014101035" @default.
- W1945885800 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4769187" @default.
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