The Small Non-coding RNA MicC is a Critical Regulator of the Stress Resistance and Virulence of Extraintestinal Pathogenic Escherichia coli

Here, we used a series of deletion strains to probe a panel of seven conserved sRNAs (DsrA, RprA, OxyS, RyhB, MicF, MicC, and Spot 42) of Extraintestinal Pathogenic Escherichia coli (ExPEC) isolate UTI89 for effects on the response to oxidative stress. ExPEC strains are the primary etiologic agents of urinary tract infections, which consistently rank among the most common infectious diseases and are a leading cause of sepsis.

In broth culture, each sRNA deletion knockout grew like the wild-type strain, whereas the spot42 (spf) and micC knockout strains were both markedly impaired in their ability to deal with oxidative stress generated by methyl viologen. UTI89ΔmicC had several additional in vitro and in vivo phenotypes important for pathogenesis. in vitro, the micC knockout had impaired motility, reduced association with and survival within bladder epithelial cells (BECs), and reduced resistance to human serum. in vivo, the micC knockout was defective in its ability to colonize and persist in the mouse urinary tract, gastrointestinal tract, and bloodstream.