Table 2:

Therapeutic uses of SPMs in animal models of lung disease influenced by air pollution and smoking exposures

Lipid/Lipid Modifier	In vivo model	Result	Reference
EPA	Allergic airways inflammation to house dust mite antigen	MSCs pre-treated with EPA suppressed inflammation and produced elevated levels of SPMs	(Abreu, et al., 2018)
DHA	Instillation of agricultural dust	Dietary DHA reduced BAL neutrophil influx and pro-inflammatory cytokines	(Nordgren, et al., 2014)
DHA	Instillation of agricultural dust	Mice on a high-DHA diet were protected from inflammation and exhibited increased levels of the repair protein amphiregulin	(Nordgren, Heires, et al., 2018)
Omega-3 PUFA	RCT of omega-3 PUFA supplementation in horses with chronic respiratory disease	Supplementation increased plasma levels of DHA and significantly reduced clinical symptoms compared to a low-dust diet alone	(Nogradi, et al., 2015)
MaR1	Instillation of agricultural dust	Pretreatment with MaR1 by i.p. injection attenuated tissue inflammation, BAL neutrophil influx, and pro-inflammatory cytokine production	(Nordgren, et al., 2015)
RvD1	Acute cigarette smoke exposure	RvD1 given by inhalation reduced cigarette smoke-induced inflammation, and accelerated resolution of inflammation when given after smoking cessation	(Hsiao, et al., 2013)
AT-RvD1	Chronic cigarette smoke exposure	AT-RvD1 given by inhalation or i.v. injection inhibited emphysematous changes in lung architecture, and reduced lung inflammation, oxidative stress and apoptosis	(Hsiao, et al., 2015)
RvD1	Chronic cigarette smoke exposure	RvD1 inhibited structural emphysema and inflammation when given concurrently with smoke exposure, and promoted lung tissue regeneration when given after smoking cessation	(Kim, et al., 2016)
AT-RvD1	Chronic cigarette smoke exposure	AT-RvD1 promoted tissue repair by upregulating the Nrf2/Keap1 pathway	(Posso, et al., 2018)
LXA4	Urban particulate matter exacerbation of allergic airway inflammation (asthma)	LXA4 inhibited tissue inflammation, BAL eosinophils, Th2 cytokines, and expression of Th2 transcription factors	(Lu, et al., 2018)
Soluble epoxide hydrolase inhibitor (sEHI) t-TUCB	Mouse OVA model of allergic airway inflammation	t-TUCB increased tissue levels of anti-inflammatory EETs and reduced inflammation, eosinophils and Th2 cytokines	(Yang, et al., 2015).
sEHI GSK2256294A	Acute cigarette smoke exposure	GSK2256294A inhibited BAL neutrophilia and lung tissue CXCL1	(Podolin, et al., 2013).

Abbreviations:

AT-RvD1, aspirin-triggered resolvin D1

BAL, bronchoalveolar lavage

DHA, docosahexaenoic acid

EET, Epoxyeicosatrienoic acids

EPA, eicosapentaenoic acid

LXA₄, lipoxin A₄

MaR1, maresin 1

MSC, mesenchymal stem cells or mesenchymal stromal cells

PUFA, polyunsaturated fatty acids

RCT, randomized controlled trial

RvD1, resolvin D1

RvD2, resolvin D2

sEHI, soluble epoxide hydrolase inhibitor

t-TUCB, trans-4-{4-[3-(4-Trifluoromethoxyphenyl)ureido]cyclohexyloxy}benzoic acid