TviA reduces T3SS-1-dependent, flagellin-independent inflammatory responses in the cecal mucosa.

<p>(A) HeLa 57A cells were infected with an aflagellate SL1344 <i>fliC fljB</i> mutant (SW762), a <i>fliC fljB phoN</i> mutant (SW793), a <i>fliC fljB phoN</i>::<i>tviA</i> mutant (SW764) and derivatives carrying an additional mutation in <i>invA</i> (SW794; SW766). NF-κB activation was determined as described above. (B and C) Groups of streptomycin-pretreated C57BL/6 mice were intragastrically inoculated with either a <i>S.</i> Typhimurium SL1344 <i>fliC fljB phoN</i> mutant (N = 8), a <i>fliC fljB phoN</i>::<i>tviA</i> mutant (N = 8), a <i>fliC fljB phoN invA</i> mutant (N = 4), a <i>fliC fljB phoN</i>::<i>tviA invA</i> mutant (N = 4), or LB broth (mock-treated; N = 3). 12 h after infection, the relative abundance of <i>Nos2</i> (B) and <i>Tnfa</i> (C) mRNA was determined by qRT-PCR. Bars represent geometric means ± standard error. *, <i>P</i><0.05; **, <i>P</i><0.01; ns, not statistically significant.