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, 2010). Indeed, these observations suggest on the atheroprotective effects of human colonic commensal bacteria. Increased intestinal microbiota-derived lipopolysaccharide (LPS) load from the colon lumen was shown to be associated with various metabolic abnormalities including induction of adipose inflammation and insulin resistance (Cani et al., 2007). Bacterial LPS could be delivered from the gut to the circulation through chylomicron-associated transport and via tight junctions in the epithelial lining (Caesar et al., 2010). LPS is absorbed by enterocytes and transferred to the Golgi apparatus where chylomicrons synthesized by enterocytes are stored before secretion (Sabesin and Frase, 1977). Inhibition of chylomicron formation suppressed intestinal LPS absorption (Ghoshal et al., 2009). High-fat meal intake increases circulating levels of LPS (Amar et al., 2008). Enhanced LPS load across the tight junctions of the gut epithelium was observed in animal models of human obesity and associated with the rearrangement of tight junction proteins, reduced epithelial barrier function, and increased gut permeability, endotoxemia, and inflammation (Brun et al., 2007; Cani et al., 2008). Administration of antibiotics or prebiotic oligofructose was shown to improve the integrity of intestinal epithelium and decrease serum low density lipoproteins (LDLs) and liver inflammation (Cani et al., 2009). Similarly, treatment of ApoE-null mice with a mixture of eight probiotics VSL#3 had anti-inflammatory effects on the gastrointestinal tract by decreasing aortic atherosclerosis, steatohepatitis, and low-grade inflammation of intestinal and mesenteric adipose tissues induced by a high-fat cholesterol intake (Mencarelli et al., 2012). PI3K inhibitor Therefore, high-fat food leads to unfavorable changes in gut microbiota that contributes to induction of metabolic abnormalities in the host organism associated with primary intestinal epithelial dysfunction and induction of gastrointestinal inflammation that could be reversed by administration of probiotics and their products (Lee, 2013). It is essential to note here that ApoE mice naturally develop atherosclerotic plaque even in the absence of high fat diet (HFD); however, HFD accelerates this process (Imaizumi, 2011). Gut Microbiota and Phosphatidylcholine Metabolism Recently, a proatherogenic role of the gut microbiota in the metabolism of phosphatidylcholine was shown (Wang et al., 2011b). Intestinal microbiota metabolizes choline and phosphatidylcholine to trimethylamine (TMA), which is further converted to a proatherogenic compound, trimethylamine-N-oxide (TMAO; Koeth et al., 2013). Dietary L-carnitine, a TMA abundant in red meat, is metabolized by intestinal microbiota to TMAO and accelerates atherosclerosis in ApoE-null mice through changes in microbial composition and increased colon production of TMA and TMAO (Ferguson, 2013). The production of TMAO was dependent on variability of the gut microbiota species.