Review of methodology and re-analysis of lipidomic data focusing on Specialised Pro-Resolution Lipid Mediators (SPMs) in a human model of resolving inflammation.

Using a model of UV-killed E. coli driven dermal inflammation in healthy human volunteers,<br/>we originally reported that following inflammatory resolution there was the infiltration of <br/>macrophages, which, through prostanoids including prostaglandin (PG)E2, imprints long-term <br/>tissue immunity. In addition to the prostanoids, data on levels of Specialised Pro-Resolution <br/>Lipid Mediators (SPMs) throughout inflammatory onset, resolution and post-resolution phases<br/>of this model were presented, but as illustrations rather than as primary data. Therefore, in <br/>response to a request for increased transparency, a subset of the original data from our human UV-killed E. coli model were re-analysed by two experts from an independent laboratory alongside a review of the methodology used. The prostanoids were robustly detected following re-analysis but the areas of the chromatographic peaks of the SPM lipid mediators were too small to yield amounts that could be reliably detected and/or quantified using community standards. Importantly, with prostanoids including PGE2 being robustly detected, this reanalysis does not alter the original report that post-resolution PGs imprint tissue immunity.Here we show the outcome of this re-analysis and review the biology surrounding SPMs as a result.