Escherichia coli diarrhea genic are human pathogens which may progress to deadly serious diseases, thus they have been studied to better understand their pathogenic mechanisms. These bacteria have on their genome the Locus of Enterocyte Effacement (LEE) pathogenicity island, responsible to encode for many virulence factors, amongst them a Type 3 Secretion System. The 2 histidine kinase sensors, QseC and QseE regulate directly the LEE expression, and other virulence mechanisms developed by these pathogens, and these sensors respond to hormones epinephrine (Epi) and norepinephrine (NE), and the autoinducer 3 (AI-3) secreted by bacteria. Diarrhea genic E. coli are natural pathogens of humans who do not have an animal model widely accepted in literature, limiting the in vivo studies of QseC and Qsee sensors. Citrobacter rodentium is a natural murine pathogen, which exhibit homology of 67% of their genes with these human pathogens, including LEE. For these characteristics, C. rodentium becomes an alternative model of in vivo studies for samples that have LEE. For a better understanding of QseC and QseE sensors, will be developed a study of the chemical signals these sensors in Citrobacter rodentium, for such will be made the construction of mutants qseC , qseE and qseC/qseE, and then the phenotypic characterization of mutants through the test cell adhesion, motility test, FAS test, for identification of attaching and effacing lesion (A/E) and chemical signaling test by epinephrine and norepinephrine. A better understanding of these sensors in C. rodentium may assist in vivo studies for the development of new drugs and therapies for the treatment of bacterial infections in the future.
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