Bacteria need iron, and as soon as they invade the human body, they are on the hunt for it. There is a limited supply of iron inside the human body where it is stored by the proteins tranferrin and ferritin.
Disease-causing bacteria have evolved by producing siderophores which are iron-chelating molecules. These molecules can bind to iron stored in ferritin and transferrin and "steal" it for the bacteria.
In this new study, the authors compared Escherichia coli taken from it's natural habitat in the gut and compared it to E. coli found in the urinary tracts of subjects suffering from urinary tract infections (UTIs). They found "epigenetic optimization" of the E. coli from the urinary tract:
Urinary tract infections (UTIs) are among the most common bacterial infections treated by physicians worldwide. Although symptoms of acute infection are often resolved with a course of antibiotics, the same bacterial strain often causes subsequent bouts of symptomatic infection. Escherichia coli are the most common bacteria causing UTI and the infecting strains are widely believed to originate from the gastrointestinal tract where multiple E. coli strains reside. Here, we use a novel mass spectrometric technique in a population of patients with recurrent UTI to identify how strains that cause UTI differ from other strains that were present in the gastrointestinal tract at the same time. We found that urinary E. coli strains preferentially expressed two small molecules called yersiniabactin and salmochelin. These molecules are called siderophores, meaning they are able to scavenge iron to support bacterial survival and growth. Synthesis and transport of these small molecules requires a coordinated network of proteins encoded by a collection of different genes. These findings suggest that new antibiotics directed against yersiniabactin or salmochelin-producing E. coli strains may be an improved, and more targeted, strategy to prevent recurrent UTIs.Since some iron-transport systems also naturally transport antibiotics into the cell it is important to understand the molecular mechanism of iron transport here. Understanding these pathogenic bacteria may lead to new ways of either delivering or designing drugs which exploit this difference.
Many of us with Cushing's Syndrome/Disease (even if in remission) suffer from low ferritin. When we have an infection, due to our compromised immune system, we often have a difficult time recovering. When accounting for the iron-depleting nature of our infections, we are doubly plagued.
To read more:
- How some bacteria may steal iron from their human host
- Acquisition of siderophores in Gram-negative bacteria
- Pathogenic E. coli
Jeffrey P. Henderson, Jan R. Crowley, Jerome S. Pinkner, Jennifer N. Walker, Pablo Tsukayama, Walter E. Stamm, Thomas M. Hooton, Scott J. Hultgren (2009). Quantitative Metabolomics Reveals an Epigenetic Blueprint for Iron Acquisition in Uropathogenic Escherichia coli PLoS Pathogens, 5 (2) DOI: 10.1371/journal.ppat.1000305