T3SS1 effectors suppress NLRC4-mediated inflammasome activation.

<p>BMMs from wild-type, NLRP3-deficient (<i>Nlrp3</i>^−/−), or NLRC4-deficient (<i>Nlrc4</i>^−/−) mice were primed with LPS and infected with <i>V. parahaemolyticus</i> mutant, Δ<i>tdhAS</i> or Δ<i>tdhAS</i>Δ<i>h1</i>in which the effectors' genes are deleted. <b>A.</b> Schematic representation of gene structure in the h1 region of T3SS1. <b>B.</b> Activation of caspase-1 and IL-1β processing in infected BMMs were analyzed using immunoblotting with anti-caspase-1 or anti-IL-1β antibody. <b>C.</b> IL-1β secretion into culture supernatants from infected BMMs at 3 hpi. was analyzed using an ELISA. Data are presented as the means ± SD of triplicate samples. *p<0.05. <b>D.</b> Culture supernatants from infected BMMs were analyzed for LDH release. Data are presented as the means ± SD of triplicate samples. *p<0.05.