Abstract / Description of output
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, data on levels of Specialised Pro-Resolution
Lipid Mediators (SPMs) throughout inflammatory onset, resolution and post-resolution phases
of this model were presented, but as illustrations rather than as primary data. Therefore, in
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.
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, data on levels of Specialised Pro-Resolution
Lipid Mediators (SPMs) throughout inflammatory onset, resolution and post-resolution phases
of this model were presented, but as illustrations rather than as primary data. Therefore, in
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.
Original language | English |
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Journal | International Journal of Experimental Pathology |
Publication status | Published - 23 Dec 2024 |