Lipidomic analysis reveals differences in Bacteroides species driven largely by plasmalogens, glycerophosphoinositols and certain sphingolipids

There has been increasing interest in bacterial lipids in recent years due, in part, to their emerging role as molecular signalling molecules. Bacteroides thetaiotaomicron 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. B. thetaiotaomicron 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 4 species of gut associated Bacteroides . In total we identify 170 different lipids and we report that the range and diversity of Bacteroides lipids is species-specific. Multi-variate analysis reveals that the differences in the lipid signatures are largely driven by the presence/absence of plasmalogens, glycerophosphoinositols and certain SP. Moreover, we show that, in B. thetaiotaomicron , mutations altering either SP or glycine lipid biosynthesis results in significant changes in the levels of other lipids suggesting the existence of compensatory mechanisms required to maintain the functionality of the bacterial membrane. Importance Bacteroides are important beneficial members of the gut microbiome that produce lipids that can function as cross-kingdom signalling molecules. We describe, for the first time, a comprehensive and qualitative comparison of the lipid signatures of 4 important Bacteroides species. We identify a group of Bacteroides core lipids and uncover species-specific differences in plasmalogen, glycerophospholipid and SP metabolism with more subtle differences observed in glycine lipid production. This data will provide a useful platform for the further characterisation of the lipid-based host-microbe dialogue and the influence of microbial lipids on host health and disease states. ### Competing Interest Statement The authors have declared no competing interest.