TLR4 and serum lipopolysaccharide activity: Activating TLR-4 in vessels with bacterial products like LPS increases NADPH oxidase-dependent O2− production and inflammation.52 In SLE mice, plasma endotoxin levels were increased, and intervention addressed to reduce endotoxemia normalized vascular TLR-4 expression and improved both vascular oxidative stress and inflammation.17,21 In addition, we were able to find increased LPS plasma levels in SLE mice associated with lower colonic integrity.