Figure 1.

Endogenous PCTR1 is up-regulated during the resolution phase of acute inflammation. A: Self-resolving inflammation was induced in mice by injecting Escherichia coli (1 × 10⁵ colony forming units; i.p.). Exudates were collected, products were extracted with the use of C18 solid-phase extraction, and lipid mediators were profiled with lipid mediator metabololipidomics. Representative multiple reaction monitoring chromatogram and MS-MS spectra were used in the identification of PCTR1. B: Time course for quantification of PCTR1 in E. coli–infected mouse exudates measured by liquid chromatography MS-MS. Representative dot plot for fluorescence-activated cell sorting exudate leukocyte composition taken at 12, 24, and 48 hours is shown, with gates showing percentage of peritoneal macrophage (CD11b⁺ F4/80⁺ Ly6G⁻) frequency (7%, 17%, and 36%). C: PCTR1 biosynthetic pathway. DHA is converted by lipoxygenase to 17S-hydroperoxy intermediate that is rapidly transformed to a 16S,17S-epoxide intermediate that undergoes conjugation to produce PCTR1.⁶ Data are expressed as means ± SEM (B). n = 4 experiments (4 to 6 mice per experiment). *P ≤ 0.05, t-test. DHA, docosahexaenoic acid; m/z, mass to charge ratio; MS-MS, tandem mass spectrometry; PCTR, protectin conjugates in tissue regeneration; Q1, parent ion; Q3, diagnostic daughter ion.