Re-analysis of lipidomic data reveals Specialised Pro-Resolution Lipid Mediators (SPMs) to be lower than quantifiable limits of assay in a human model of resolving inflammation.

Abstract

Using a model of UV-killed E. coli driven dermal inflammation in healthy human volunteers we originally reported that following inflammatory resolution there was the infiltration of macrophages, which, through prostanoids including prostaglandin (PG)E2, imprints long-term tissue immunity. In addition to the prostanoids, we also presented data on levels of Specialised Pro-Resolution Lipid Mediators (SPMs) throughout inflammatory onset, resolution and post-resolution phases of this model. However, our collaborators who carried out the lipidomic analysis received a complaint concerning how they generally present SPM data in their publications, namely their use of graphical illustrations to depict data. Importantly, such lipidomic illustrations were used in our human UV-killed E. coli study. Therefore, in the interest of transparency and to replace these illustrations with more meaningful images, the original data from our human UV-killed E. coli model were re-analysed by two independent experts. It transpires that the integrated areas of the chromatographic peaks of the SPM lipid mediators were below the amounts that could be reliably either detected and/or quantified using community standards for quantitation. Here we show the outcome of this reanalysis. Importantly, with prostanoids including PGE2 being robustly detected, this re-analysis does not alter the original report that post-resolution PGs imprint tissue immunity.