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脂质组学分析揭示了物种间的差异,这些差异主要由缩醛磷脂、甘油磷酸肌醇和某些鞘脂驱动。

Lipidomic Analysis Reveals Differences in Species Driven Largely by Plasmalogens, Glycerophosphoinositols and Certain Sphingolipids.

作者信息

Ryan Eileen, Gonzalez Pastor Belén, Gethings Lee A, Clarke David J, Joyce Susan A

机构信息

APC Microbiome Ireland, University College Cork, T12 K8AF Cork, Ireland.

School of Biochemistry & Cell Biology, University College Cork, T12 K8AF Cork, Ireland.

出版信息

Metabolites. 2023 Feb 28;13(3):360. doi: 10.3390/metabo13030360.

DOI:10.3390/metabo13030360
PMID:36984802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10056535/
Abstract

There has been increasing interest in bacterial lipids in recent years due, in part, to their emerging role as molecular signalling molecules. is an important member of the mammalian gut microbiota that has been shown to produce sphingolipids (SP) that pass through the gut epithelial barrier to impact host SP metabolism and signal into host inflammation pathways. also produces a novel family of N-acyl amines (called glycine lipids) that are potent ligands of host Toll-like receptor 2 (TLR2). Here, we specifically examine the lipid signatures of four species of gut-associated . In total we identify 170 different lipids, and we report that the range and diversity of lipids is species specific. Multivariate analysis reveals that the differences in the lipid signatures are largely driven by the presence and absence of plasmalogens, glycerophosphoinositols and certain SP. Moreover, we show that, in , mutations altering either SP or glycine lipid biosynthesis result in significant changes in the levels of other lipids, suggesting the existence of a compensatory mechanisms required to maintain the functionality of the bacterial membrane.

摘要

近年来,人们对细菌脂质的兴趣与日俱增,部分原因在于其作为分子信号分子的新作用。[具体细菌名称]是哺乳动物肠道微生物群的重要成员,已被证明能产生鞘脂(SP),这些鞘脂穿过肠道上皮屏障,影响宿主的SP代谢,并向宿主炎症途径发出信号。[具体细菌名称]还产生了一个新的N - 酰基胺家族(称为甘油脂),它们是宿主Toll样受体2(TLR2)的有效配体。在此,我们专门研究了四种肠道相关[具体细菌名称]的脂质特征。我们总共鉴定出170种不同的脂质,并报告[具体细菌名称]脂质的范围和多样性具有物种特异性。多变量分析表明,脂质特征的差异很大程度上是由缩醛磷脂、甘油磷酸肌醇和某些SP的存在与否所驱动的。此外,我们表明,在[具体细菌名称]中,改变SP或甘油脂生物合成的突变会导致其他脂质水平的显著变化,这表明存在维持细菌膜功能所需的补偿机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/32a8e3393f8e/metabolites-13-00360-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/b12bc3393b62/metabolites-13-00360-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/9f3ba5bbfd3c/metabolites-13-00360-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/580d8418616f/metabolites-13-00360-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/1202fbe4ed33/metabolites-13-00360-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/5a4eb4fa9259/metabolites-13-00360-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/32a8e3393f8e/metabolites-13-00360-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/b12bc3393b62/metabolites-13-00360-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/9f3ba5bbfd3c/metabolites-13-00360-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/580d8418616f/metabolites-13-00360-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/1202fbe4ed33/metabolites-13-00360-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/5a4eb4fa9259/metabolites-13-00360-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/789c/10056535/32a8e3393f8e/metabolites-13-00360-g006.jpg

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