Salmonella enterica, one of the main causes of gastrointestinal infections, modulates its virulence gene expression, adapting it to each stage of the infection process, depending on the free iron concentration found in the intestinal epithelium of its host. Researchers at Universitat Autnoma de Barcelona (UAB) have demonstrated for the first time that the pathogen activates these genes through the Fur protein, which acts as a sensor of iron levels in its surroundings.
The research, published online in the journal PLoS ONE and entitled "Fur activates the expression of Salmonella enterica pathogenicity island 1 by directly interacting with the hilD operator in vivo and in vitro", was carried out by the Molecular Microbiology Group of the UAB Department of Genetics and Microbiology and coordinated by Dr Jordi Barb. Dr Juan Carlos Alonso from the National Biotechnology Centre also collaborated in the research group.
Iron is an essential part of the development of almost all living organisms. This is why all organisms have developed an iron uptake system which guarantees that they can acquire it from their external environment. However, too much iron in the cell interior can have harmful effects and organisms have systems to control this as well.
In vertebrates, this control produces a first defence barrier known as nutritional immunity which limits the amount of free iron found in biological fluids and prevents the development of pathogens. Only the upper intestinal track, given its anaerobic condition, presents appreciable levels of free iron. In the majority of gram-negative bacteria, such as Salmonella enterica, the control of iron levels is carried out by the Fur protein (Ferric Uptake Regulator), which interacts with the DNA and adjusts the production of uptake and storage systems of this element to the cell's cytoplasm.
Salmonella enterica is one of the most common bacterial pathogens
|Contact: Maria Jesus Delgado|
Universitat Autonoma de Barcelona