Protectins and maresins: New pro-resolving families of mediators in acute inflammation and resolution bioactive metabolome.
Level 5 - mechanism / opinion, no new human data
Narrative review of biochemical pathways, cell biology, and animal disease models.
PubMed 25139562 · doi:10.1016/j.bbalip.2014.08.006
What was done
The authors reviewed the identification, stereochemical assignment, biosynthesis, and in vivo actions of protectins (including protectin D1/neuroprotectin D1) and maresins (MaR1 and MaR2). The review examines data from systems approaches involving self-resolving inflammatory exudates in mice and human leukocyte preparations metabolizing docosahexaenoic acid (DHA) and other n-3 essential fatty acids.
What was found
The abstract reports no clinical numbers or pooled statistical data. It describes that human leukocytes and inflammatory exudates convert DHA via epoxide intermediates into distinct families of di- and trihydroxy-containing mediators (D-series resolvins D1–D6, protectins, and maresins MaR1/MaR2) that act stereoselectively at picogram amounts. Aspirin triggers an endogenous pathway yielding aspirin-triggered neuroprotectin D1/protectin D1 [AT-(NPD1/PD1)] to stimulate resolution in preclinical models of infection, inflammatory pain, tissue regeneration, neuroprotection, and wound healing.
Why it matters
This work details the biochemical pathways showing that inflammation resolution is an active, receptor-mediated biological process driven by specialized pro-resolving lipid mediators derived from essential fatty acids.
Limits
The abstract describes a narrative review of bench chemistry, in vitro human leukocyte preparations, and animal disease models. No clinical human trial data, quantitative effect estimates, sample sizes, or systematic review search methodologies are provided.
Cited by
- supports EPA is metabolized into E-series resolvins, while DHA is metabolized into D-series resolvins, protectins, and neuroprotectins.