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Lipidomic Profiling in Inflammatory Bowel Disease: Comparison Between Ulcerative Colitis and Crohn's Disease
Fenling Fan1, Piyushkumar A Mundra, Lu Fang
1*Baker IDI Heart and Diabetes Institute, Melbourne, Australia; †Department of Cardiovascular Medicine, The Alfred Hospital, Melbourne, Australia; ‡Department of Cardiovascular Medicine, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China; and §Departments of Gastroenterology, The Alfred Hospital, Melbourne, Australia.
Background:
Inflammatory bowel disease (IBD), which encompasses ulcerative colitis (UC) and Crohn's disease (CD), is believed to be caused by abnormal host immune responses to the intestinal microbiome. However, the precise etiology of IBD remains unknown. Lipid metabolism and signaling are suggested to play important roles in inflammation with significant implications for IBD. In this study, we aimed to characterize lipidomic profiles in IBD with comparison between healthy controls, UC, and CD.
Methods:
Patients with IBD (n = 40, UC: 16 and CD: 24) and age- and gender-matched healthy volunteers (n = 84) were recruited. Plasma lipid profiles containing 333 lipid species were measured using electrospray ionization-tandem mass spectrometry.
Results:
A total of 86 individual lipid species were significantly changed in CD compared with controls (78 decreased while 8 increased), with the majority belonging to the ether lipids including the alkylphospholipids (alkylphosphatidylcholine and alkylphosphatidylethanolamine) and plasmalogens (alkenylphosphatidylcholine and alkenylphosphatidylethanolamine). Of these 86 lipid species, 33 remained significantly and negatively associated with CD after adjusting for age, sex, waist circumference, current smoking, and diastolic blood pressure in logistic regression. In contrast, only 5 lipid species significantly differed between UC and controls.
Conclusions:
We demonstrate that a number of ether lipids (alkylphospholipid and plasmalogens) are significantly and negatively associated with CD. These alterations of lipid profiles particularly plasmalogens may contribute to the pathogenesis of IBD.
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