Fan Fenling, Mundra Piyushkumar A, Fang Lu, Galvin Abby, Moore Xiao Lei, Weir Jacquelyn M, Wong Gerard, White David A, Chin-Dusting Jaye, Sparrow Miles P, Meikle Peter J, Dart Anthony M
*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.
Inflamm Bowel Dis. 2015 Jul;21(7):1511-8. doi: 10.1097/MIB.0000000000000394.
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.
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.
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.
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.
炎症性肠病（IBD）包括溃疡性结肠炎（UC）和克罗恩病（CD），被认为是由宿主对肠道微生物群的异常免疫反应引起的。然而，IBD的确切病因仍不清楚。脂质代谢和信号传导被认为在炎症中起重要作用，对IBD有重大影响。在本研究中，我们旨在通过比较健康对照、UC和CD来表征IBD中的脂质组学特征。
招募了IBD患者（n = 40，UC：16例，CD：24例）以及年龄和性别匹配的健康志愿者（n = 84）。使用电喷雾电离串联质谱法测量包含333种脂质种类的血浆脂质谱。
与对照组相比，CD中共有86种个体脂质种类发生了显著变化（78种减少而8种增加），其中大多数属于醚脂，包括烷基磷脂（烷基磷脂酰胆碱和烷基磷脂酰乙醇胺）和缩醛磷脂（烯基磷脂酰胆碱和烯基磷脂酰乙醇胺）。在逻辑回归中调整年龄、性别、腰围、当前吸烟情况和舒张压后，这86种脂质种类中有33种仍与CD显著负相关。相比之下，UC和对照组之间只有5种脂质种类有显著差异。
我们证明了许多醚脂（烷基磷脂和缩醛磷脂）与CD显著负相关。这些脂质谱的改变，尤其是缩醛磷脂，可能有助于IBD的发病机制。
