Lipids in Health and Disease · 7 authors, 5 centres
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Conventionally raised, antibiotic-treated, and germ-free mice were given DNBS to induce colitis, and germ-free mice exhibited reduced colonic inflammation alongside elevated levels of anti-inflammatory endocannabinoidome lipid mediators. These findings suggest that the absence of gut microbiota leads to compensatory increases in protective lipid mediators that may partly account for lower colitis susceptibility.
Colitis was induced in conventionally raised, antibiotic-treated, and germ-free mice using DNBS, and inflammation was assessed by disease activity index, body weight change, colon weight-length ratio, MPO activity, cytokine gene expression, and HPLC-MS/MS-measured colonic eCBome lipid mediators. GF mice showed elevated baseline levels of anti-inflammatory eCBome lipids including OEA, LEA, DHEA, and 13-HODE-EA. Following DNBS treatment, GF mice exhibited lower colon weight-length ratios and reduced expression of Il1b, Il6, Tnfa, and neutrophil markers compared to CR and ABX groups. MPO activity did not increase in DNBS-treated GF or ABX mice, and Il10 expression was lower in GF mice at baseline. Levels of several N-acyl ethanolamines and 13-HODE-EA were higher in DNBS-treated GF mice and negatively correlated with measures of colitis. Results suggest that microbiota depletion alters eCBome signalling in a manner that may partially protect against DNBS-induced colonic inflammation.
