Fig. 8: SIRT2 restricts Shigella infection in cell and in vivo by counteracting IcsB.
From: Golgi stress induces SIRT2 to counteract Shigella infection via defatty-acylation
A Effect of SIRT2 knockout and IcsB deletion on S. flexneri intracellular proliferation. MOI were determined after 10 min of infection and 6 h of incubation in the presence of 50 μg/ml gentamicin. Data are represented as mean ± SEM with three biological replicates. Statistical evaluation was done by two-way ANOVA. B CFU in lung homogenates from Sirt2+/+ and Sirt2−/− C57BL/6 J mice infected with wildtype or IcsB deletion S. flexneri M90T for 3 days. Data are presented as mean ± SEM with three mice per group. Statistical evaluation was done using two-way ANOVA. C CFU in lung homogenates from Sirt2+/+ and Sirt2−/− C57BL/6 J mice infected with wildtype or IcsB deletion S. flexneri M90T rescued with WT or C306A IcsB for 3 days. n = 4–9 biological replicates. Data are presented as mean ± SEM with at least three mice per group. Statistical evaluation was done using two-way ANOVA. D Model depicting SIRT2 as a Golgi stress response protein that limits Shigella pathogenesis by counteracting Shigella-mediated host protein lysine fatty acylation. ***p < 0.001.
