Table 1:

In vitro studies of SPMs in lung cells suggesting therapeutic potential

Lipid/Lipid modifier	Targets	Mechanism	Cell types reported	Reference
EPA, DHA		Increased production of pro-resolution lipid mediators; increases recellularization of lung scaffolds	MSCs, lung fibroblasts, epithelial cells and monocytes	(Abreu, et al., 2018; Nordgren, et al., 2014; Nordgren, Heires, et al., 2018)
RvD1 and AT-RvD1	GPR32, ALX/FPR2	Reduce inflammatory cytokines, increase macrophage phagocytosis and M2 phenotype, reduce NF-κB, STAT6, STAT1, TAK1, TBK signaling	Macrophages, Lung fibroblasts, bronchial epithelial cells, small airway epithelial cells	(Croasdell, et al., 2015; de Oliveira, et al., 2017; Hsiao, et al., 2013; Hsiao, et al., 2014)
RvD2	GPR32, ALX/FPR2	Reduce inflammatory cytokines, increase phagocytosis in macrophages exposed to cigarette smoke extract	Macrophages	(Croasdell, et al., 2015)
MaR1	Serum Response element signaling	Reduction of IL-6 and IL-8, lowered neutrophil accumulation, IL-6 and TNFα levels in BAL	Bronchial epithelial cells	(Nordgren, et al., 2013)
Protectin		Increased differentiation of macrophages, increased efferocytosis/phagocytosis	Monocytes, macrophages	(Pistorius, et al., 2018)
Soluble epoxide hydrolase inhibitors (sEHIs)	Soluble epoxide hydrolase	Reduced breakdown of pro-resolution lipid mediators	Ex vivo analysis of human and rodent blood, serum, sputum and BAL cells	(Ono, et al., 2014; Podolin, et al., 2013).

Abbreviations:

AT-RvD1, aspirin-triggered resolvin D1

BAL, bronchoalveolar lavage

DHA, docosahexaenoic acid

EPA, eicosapentaenoic acid

MaR1, maresin 1

MSC, mesenchymal stem cells or mesenchymal stromal cells

RvD1, resolvin D1

RvD2, resolvin D2

sEHI, soluble epoxide hydrolase inhibitor