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. The gene discussed is FMO5; the disease is serum lipopolysaccharide activity.