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. Author manuscript; available in PMC: 2016 Apr 8.
Published in final edited form as: Cell Host Microbe. 2015 Mar 26;17(4):429–440. doi: 10.1016/j.chom.2015.03.001

Figure 4. Susceptibility to S. aureus Conferred by Autophagy Deficiency Is Dependent on Bacterial α-toxin Production.

Figure 4

(A) WT and Atg16L1HM mice were injected i.v. with 107 or 108 cfu USA300 Δagr. n=10 mice/group. Data represent 2 independent experiments.

(B) Western blot analysis of USA300, USA300 Δhla, USA400, and USA500 using an anti-α-toxin antibody. MW indicates molecular weight protein marker, WT indicates isogenic wild type USA300, asterisk indicates a non-specific, anti-α-toxin cross-reactive band.

(C) WT and Atg16L1HM mice were infected i.v. with 107 cfu USA300 or USA300 Δhla. n=7–15 mice/group. Data represent 2 independent experiments. *p<0.05 comparing Atg16L1HM + USA300 versus Atg16L1HM + USA300 Δhla.

(D) WT and Atg16L1HM mice were infected i.v. with 108 cfu USA300 or USA300 Δhla. n=7–15 mice/group. Data represent 4 independent experiments. ****p<0.0001 comparing Atg16L1HM + USA300 versus Atg16L1HM + USA300 Δhla and ****p<0.0001 comparing Atg16L1HM + USA300 Δhla versus WT + USA300 Δhla.

(E) WT and Atg16L1HM mice were inoculated intranasally with 108 cfu USA300 Δhla transformed with either empty plasmid (USA300 Δhla+EV) or a plasmid overexpressing hla (USA300 Δhla+phla). n=8–14 mice/group. Data represent 3 independent experiments. *p<0.05 comparing WT + USA300 Δhla+EV with WT + USA300 Δhla+phla. ***p<0.001 comparing Atg16L1HM + USA300 Δhla+EV with Atg16L1HM + USA300 Δhla+phla.

HHS Vulnerability Disclosure