Chylomicrons promote intestinal absorption of lipopolysaccharides Published, JLR Papers in Press, September 24, 2008.
By S. Ghoshal, J. Witta, Jian Zhong, W. D. de Villiers, E. Eckhardt. Journal of Lipid Research, 2009
631 citations recorded by the source corpus.
Recent data suggest that dietary fat promotes intestinal absorption of lipopolysaccharides (LPS) from the gut microflora, which might contribute to various inflammatory disorders. The mechanism of fat-induced LPS absorption is unclear, however. Intestinal-epithelial cells can internalize LPS from the apical surface and transport LPS to the Golgi. The Golgi complex also contains newly formed chylomicrons, the lipoproteins that transport dietary long-chain fat through mesenteric lymph and blood. Because LPS has affinity for chylomicrons, we hypothesized that chylomicron formation promotes LPS absorption. In agreement with our hypothesis, we found that CaCo-2 cells released more cell-associated LPS after incubation with oleic-acid (OA), a long-chain fatty acid that induces chylomicron formation, than with butyric acid (BA), a short-chain fatty acid that does not induce chylomicron formation. Moreover, the effect of OA was blocked by the inhibitor of chylomicron formation, Pluronic L-81. We also observed that intragastric triolein (TO) gavage was followed by increased plasma LPS, whereas gavage with tributyrin (TB), or TO plus Pluronic L-81, was not. Most intestinally absorbed LPS was present on chylomicron remnants (CM-R) in the blood. Chylomicron formation also promoted transport of LPS through mesenteric lymph nodes (MLN) and the production of TNFα mRNA in the MLN. Together, our data suggest that intestinal epithelial cells may release LPS on chylomicrons from cell-associated pools. Chylomicron-associated LPS may contribute to postprandial inflammatory responses or chronic diet-induced inflammation in chylomicron target tissues.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/6c7a4ee0c30ef8759ef59a0b3ae5dab20c8b8aea
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Citations in the corpus
- Adipokines Mediate Inflammation and Insulin Resistance (2013, neutral): “Saturated free fatty acid and gut-derived bacterial lipopolysaccharide (LPS) also bind to Toll-like receptor 4 (TLR4) to activate NF-κB and JNK and mediate inflammation and insulin resistance (Shi et al., 2006; Ghoshal et al., 2009).”
- Interactions between gut microbiota and host metabolism predisposing to obesity and diabetes. (2011, neutral): “Cell cultures and animal models suggested that endotoxin is actively secreted into the blood along with chylomicrons, and that inhibiting chylomicron synthesis blocks endotoxin secretion (89).”
- Linking Gut Microbiota and Inflammation to Obesity and Insulin Resistance. (2016, neutral): “In addition to modulation of the intestinal barrier, it has been shown that LPS is transported along with chylomicrons into the circulation, contributing to the explanation of why a high-fat diet can increase the uptake of this lipid (44).”
- Dietary Polyphenols Promote Growth of the Gut Bacterium Akkermansia muciniphila and Attenuate High-Fat Diet–Induced Metabolic Syndrome (2015, positive): “3A), suggesting higher GLP-1 and GLP-2 protein levels, which could contribute to the improved glucose tolerance and decreased presence of LPS in serum, respectively.”
- Impact of the gut microbiota on inflammation, obesity, and metabolic disease (2016, positive): “Additionally, excess fat intake triggers an increase in chylomicrons in the intestine during the postprandial period (following a meal), which favors LPS infiltration into the circulation [58].”
- Targeting gut microbiota in obesity: effects of prebiotics and probiotics (2011, background): “Several investigators have shown that intraluminal fat increases intestinal LPS absorption through its incorporation into chylomicrons”
- Understanding the Holobiont: How microbial metabolites affect human health and shape the immune system (2017, background): “Second, microbiota-derived LPS has been suggested to traverse the mucosal barrier of the intestine on chylomicrons, lipoprotein complexes that transport long-chain fatty acids from the gut lumen to the lymph and blood (Ghoshal et al., 2009; Khan et al., 2014; Sonnenburg and B€ackhed, 2016).”
- Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity (2012, background): “It has been proposed that both TLR5,(16) and TLR2,(54) knock out mice as the transport of LPS from the gut lumen toward target tissues by newly synthesized chylomicrons from epithelial intestinal cells in response to fat feeding.(29,30) We and others have confirmed these data in human subjects; ther”
- Negative Effects of a High-Fat Diet on Intestinal Permeability: A Review. (2019, background): “Although the exact mechanism was unknown at the time, it is now thought that this response is due to increased intestinal permeation of LPS, which is directly incorporated into chylomicrons and delivered to the circulatory system (86).”
- An opportunistic pathogen isolated from the gut of an obese human causes obesity in germfree mice (2012, neutral): “…of endotoxin translocation from the gut to the serum in the HFDþB29 gnotobiotic mice may be facilitated by chylomicrons induced by long-chain fatty acids in the HFD (Cani et al., 2007; Ghoshal et al., 2009), rather than by impaired gut barrier function (Cani et al., 2007; Zhang et al., 2010, 2012).”