Abstract
The lipid sensor oleoylethanolamide (OEA), an endogenous high-affinity agonist of peroxisome proliferator-activated receptor-α (PPAR-α) secreted in the proximal intestine, is endowed with several distinctive homeostatic properties, such as control of appetite, anti-inflammatory activity, stimulation of lipolysis and fatty acid oxidation. When administered exogenously, OEA has beneficial effects in several cognitive paradigms; therefore, in all respects, OEA can be considered a hormone of the gut-brain axis. Here we report an unexplored modulatory effect of OEA on the intestinal microbiota and on immune response. Our study shows for the first time that sub-chronic OEA administration to mice fed a normal chow pellet diet, changes the faecal microbiota profile, shifting the Firmicutes:Bacteroidetes ratio in favour of Bacteroidetes (in particular Bacteroides genus) and decreasing Firmicutes (Lactobacillus), and reduces intestinal cytokines expression by immune cells isolated from Peyer’s patches. Our results suggest that sub-chronic OEA treatment modulates gut microbiota composition towards a “lean-like phenotype”, and polarises gut-specific immune responses mimicking the effect of a diet low in fat and high in polysaccharides content.
Highlights
Gut microorganisms are indispensable for the regulation of the host metabolism by protecting the intestine against exogenous pathogens and potentially harmful resident microorganisms
The literature reports some discrepancies regarding how the inflammatory state in the intestine relates to obesity and metabolic diseases, some studies have shown that obesity is associated with an increased intestinal inflammation and elevated levels of intestinal TH1 and TH17 lymphocytes at the relative expense of TH2 and anti-inflammatory T regulatory (Treg) lymphocytes
We examined the consequences of sub-chronic OEA administration on the faecal microbiota profile and intestinal cytokines expression by immune cells of the mouse Peyer’s Patches
Summary
Gut microorganisms are indispensable for the regulation of the host metabolism by protecting the intestine against exogenous pathogens and potentially harmful resident microorganisms. Dysbiosis disrupts gut homeostasis and increases the risk of inflammatory responses and it is broadly accepted that changes in the microbiota are associated with intestinal[5], and immunological and metabolic diseases[6]. OEA is mobilized in the proximal intestine after a meal[27], but it is currently unclear whether it affects intestinal homeostasis by changing the profile of the microbiota and intestinal lymphocytes activity. To answer these questions, we examined the consequences of sub-chronic OEA administration on the faecal microbiota profile and intestinal cytokines expression by immune cells of the mouse Peyer’s Patches
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