APOE and atherosclerosis: Interestingly, an oral infection in apoliporotein E knockout (ApoE−/−) mice with a P. gingivalis strain expressing antagonistic lipid A caused vascular inflammation, macrophage accumulation, and progression of atherosclerosis [52], whereas a strain producing agonistic lipid A increased the levels of pro-inflammatory mediators and activated the inflammasome in a caspase-11-dependent manner.