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粪便磷脂特征会因饮食和肿瘤而改变。

Stool phospholipid signature is altered by diet and tumors.

作者信息

Davies Julie M, Hua Hong-Uyen, Dheer Rishu, Martinez Mitchell, Bhattacharya Sanjoy K, Abreu Maria T

机构信息

Division of Gastroenterology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida, United States of America.

Bascom Palmer Eye Institute, University of Miami, Miami, Florida, United States of America.

出版信息

PLoS One. 2014 Dec 3;9(12):e114352. doi: 10.1371/journal.pone.0114352. eCollection 2014.

DOI:10.1371/journal.pone.0114352
PMID:25469718
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4254978/
Abstract

Intake of saturated fat is a risk factor for ulcerative colitis (UC) and colon cancer. Changes in the microbiota have been implicated in the development of UC and colon cancer. The host and the microbiota generate metabolites that may contribute to or reflect disease pathogenesis. We used lipid class specific quantitative mass spectrometry to assess the phospholipid (PL) profile (phosphatidylcholine [PC], phosphatidylethanolamine [PE], phosphatidylinositol [PI], phosphatidylserine [PS]) of stool from mice fed a high fat (HFD) or control diet with or without induction of colitis-associated tumors using azoxymethane and dextran sodium sulfate. The microbiota was assessed using qPCR for several bacterial groups. Colitis-associated tumors were associated with reduced bulk PI and PE levels in control diet fed mice compared to untreated mice. Significant decreases in the relative quantities of several PC species were found in colitis-associated tumor bearing mice fed either diet. Statistical analysis of the PL profile revealed distinct clustering by treatment group. Partial least squares regression analysis found that the relative quantities of the PS class profile best predicted bacterial abundance of Clostridium leptum and Prevotella groups. Abundance of selected PL species correlated with bacterial group quantities. Thus, we have described that a HFD and colitis-associated tumors are associated with changes in phospholipids and may reflect host-microbial interactions and disease states.

摘要

摄入饱和脂肪是溃疡性结肠炎(UC)和结肠癌的一个风险因素。微生物群的变化与UC和结肠癌的发生有关。宿主和微生物群产生的代谢产物可能有助于或反映疾病的发病机制。我们使用脂质类特异性定量质谱法评估了喂食高脂肪(HFD)或对照饮食的小鼠粪便中的磷脂(PL)谱(磷脂酰胆碱[PC]、磷脂酰乙醇胺[PE]、磷脂酰肌醇[PI]、磷脂酰丝氨酸[PS]),这些小鼠使用氧化偶氮甲烷和葡聚糖硫酸钠诱导或未诱导结肠炎相关肿瘤。使用qPCR对几个细菌组评估微生物群。与未处理的小鼠相比,在喂食对照饮食的小鼠中,结肠炎相关肿瘤与总PI和PE水平降低有关。在喂食任何一种饮食的患有结肠炎相关肿瘤的小鼠中,发现几种PC种类的相对数量显著下降。对PL谱的统计分析显示按治疗组有明显的聚类。偏最小二乘回归分析发现,PS类谱的相对数量最能预测纤细梭菌和普雷沃菌属组的细菌丰度。选定PL种类的丰度与细菌组数量相关。因此,我们已经描述了HFD和结肠炎相关肿瘤与磷脂变化有关,并且可能反映宿主-微生物相互作用和疾病状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/230b0744c634/pone.0114352.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/0ad54992250f/pone.0114352.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/011382598d30/pone.0114352.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/d215b86b0d55/pone.0114352.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/b47a96028237/pone.0114352.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/b0dfdd36534d/pone.0114352.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/230b0744c634/pone.0114352.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/0ad54992250f/pone.0114352.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/011382598d30/pone.0114352.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/d215b86b0d55/pone.0114352.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/b47a96028237/pone.0114352.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/b0dfdd36534d/pone.0114352.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfd/4254978/230b0744c634/pone.0114352.g006.jpg

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