Impairment of IL-8 production by STM2503, STM1703 and STM4264 mutants is relieved by deletion of the biofilm regulator CsgD.

IL-8 production of HT-29 cells co-incubated with phosphodiesterase EAL-domain proteins/csgD double mutants was monitored. Restoration of immunogenicity was observed when csgD was deleted in combination with EAL-domain proteins. Overexpression of the phosphodiesterase STM3611 (p3611+ = STM3611 in pLAFR3) in the STM4264/csgD double mutant provoked no additional IL-8 production. WT = wild type S. typhimurium UMR1; VC = vector control pLAFR3; U = unstimulated HT-29 cells. Bars show mean ± standard deviation from at least three independent biological experiments performed in two technical replicates. Statistical significance is indicated by *P<0.05, **P<0.01, ***P<0.001 as compared with the respective single mutant.