| Summary: | Urinary tract infections are often polymicrobial and are mainly due to uropathogenic <i>Escherichia coli</i> (UPEC). We previously demonstrated a link among clinical fluoroquinolone susceptible <i>E. coli</i> reducing in vitro urothelial interleukin-8 (CXCL8) induced by <i>E. coli</i> K-12, polymicrobial cystitis, and pyuria absence. Here, we evaluated whether fifteen clinical fluoroquinolone susceptible UPEC were able to reduce CXCL8 induced by <i>Enterococcus faecalis</i> that had been isolated from the same mixed urines, other than CXCL8 induced by <i>E. coli</i> K-12. We also evaluated the connection between fluoroquinolone susceptibility and pathogenicity by evaluating the immune modulation of isogenic <i>gyrA</i>, a mutant UPEC resistant to ciprofloxacin. Using the 5637 bladder epithelial cell line, we observed that lower CXCL8 induced the most UPEC isolates than K-12 and the corresponding <i>E. faecalis</i>. During coinfections of UPEC/K-12 and UPEC/<i>E. faecalis</i>, we observed lower CXCL8 than during infections caused by K-12 and <i>E. faecalis</i> alone. UPEC strains showed host–pathogen and pathogen–pathogen interaction, which in part explained their persistence in the human urinary tract and coinfections, respectively. Mutant UPEC showed lower modulating activity with respect to the wildtypes, confirming the connection between acquired fluoroquinolone resistance and the decrease of innate microbial properties.
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