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Background  The neonatal meningitis  E. coli  (NMEC) strain S88 carries a ColV plasmid named pS88 which is involved in meningeal virulence. Transcriptional analysis of pS88 in human serum revealed a strong upregulation of an ORF of unknown function:  shiF,  which is adjacent to the operon encoding the siderophore aerobactin. The aim of this work is to investigate the role of  shiF  in aerobactin production in strain S88.    Results  Study of the prevalence of  shiF  and aerobactin operon in a collection of 100 extra-intestinal pathogenic  E. coli  strains (ExPEC) and 50 whole genome-sequenced  E. coli  strains revealed the colocalization of these two genes for 98% of the aerobactin positive strains. We used Datsenko and Wanner’s method to delete  shiF  in two S88 mutants. A cross-feeding assay showed that these mutants were able to excrete aerobactin meaning that  shiF  is dispensable for aerobactin excretion. Our growth assays revealed that the  shiF -deleted mutants grew significantly slower than the wild-type strain S88 in iron-depleted medium with a decrease of maximum growth rates of 23 and 28% ( p  &lt; 0.05). Using Liquid Chromatography-Mass Spectrometry, we identified and quantified siderophores in the supernatants of S88 and its  shiF  deleted mutants after growth in iron-depleted medium and found that these mutants secreted significantly less aerobactin than S88 (− 52% and - 49%,  p  &lt; 0.001).    Conclusions   ShiF  is physically and functionally linked to aerobactin. It provides an advantage to  E. coli  S88 under iron-limiting conditions by increasing aerobactin secretion and may thus act as an auxiliary virulence factor.

ShiF acts as an auxiliary factor of aerobactin secretion in meningitis Escherichia coli strain S88