Exposure of Escherichia coli to human hepcidin results in differential expression of genes associated with iron homeostasis and oxidative stress
| Autor: | Roger H. K. Morris, Delia Ripley, Jiraporn Lueangsakulthai, Michael J Pascoe, Sarah E. Maddocks |
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| Rok vydání: | 2017 |
| Předmět: |
inorganic chemicals
0301 basic medicine DNA damage Iron medicine.disease_cause Microbiology 03 medical and health sciences Hepcidins Hepcidin hemic and lymphatic diseases Genetics medicine Escherichia coli Homeostasis Humans SOS response Molecular Biology Escherichia coli Infections Regulation of gene expression biology Chemistry Escherichia coli Proteins Wild type nutritional and metabolic diseases Gene Expression Regulation Bacterial Repressor Proteins Oxidative Stress 030104 developmental biology Ferritins biology.protein bacteria Repressor lexA Oxidative stress |
| Zdroj: | FEMS microbiology letters. 365(10) |
| ISSN: | 1574-6968 |
| Popis: | Hepcidin belongs to the antimicrobial peptide family but has weak activity with regards to bacterial killing. The regulatory function of hepcidin in humans serves to maintain an iron-restricted environment that limits the growth of pathogens; this study explored whether hepcidin affected bacterial iron homeostasis and oxidative stress using the model organism Escherichia coli. Using the Miller assay it was determined that under low iron availability exposure to sub-inhibitory doses of hepcidin (4-12μM) led to 2-fold and 4-fold increases in the expression of ftnA and bfd, respectively (P < 0.05), in both a wild type (WT) and Δfur (ferric uptake regulator) background. Quantitative real-time PCR analysis of oxyR and sodA, treated with 4 or 8 μM of hepcidin showed that expression of these genes was significantly (P < 0.05) increased, whereas expression of lexA was unchanged, indicating that hepcidin likely mediated oxidative stress but did not induce DNA damage. |
| Databáze: | OpenAIRE |
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