Type I interferons give gonococci a sweet treat and a chance at survival.

In this issue, Kurt-Jones et al. demonstrate a surprising role for the type I interferon, IFN-ε, in Neisseria gonorrhoeae infections of the female reproductive tract. Rather than protecting the host, IFN-ε increases CMP-sialic acid production in epithelial cells, potentiating sialic acid modification of bacterial lipooligosaccharide, enabling innate immune evasion.