Resolvin D1 and Aspirin-Triggered Resolvin D1 Promote Resolution of Allergic Airways Responses

Rogério, Alexandre de Paula; Haworth, Oliver; Croze, Roxanne H.; Oh, Sungwhan F.; Uddin, Mohib; Carlo, Troy; Pfeffer, Michael; Priluck, Rebekah; Serhan, Charles N.; Levy, Bruce D.

doi:10.4049/jimmunol.1101665

Cited by 197 publications

(193 citation statements)

References 43 publications

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“…30,31 Resolvin D1 displays a specific activity to enhance phagocytosis in macrophages. 32,[48][49][50] We found that aspirin-triggered resolvin D1 (AT-RvD1) restored dectin-1-induced Rac1 activation in Xiap 2/2 BMDMs (supplemental Figure 11A). RvD1 did not further increase the phagocytosis of HKCA in control BMDMs but significantly increased the uptake of HKCA in Xiap 2/2 BMDMs (supplemental Figure 11B-C).…”

Section: Xiapmentioning

confidence: 92%

Inability to resolve specific infection generates innate immunodeficiency syndrome in Xiap−/− mice

Hsieh

Chuang

Chiang

et al. 2014

Blood

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Section: Xiapmentioning

confidence: 92%

Inability to resolve specific infection generates innate immunodeficiency syndrome in Xiap−/− mice

Hsieh

Chuang

Chiang

et al. 2014

Blood

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“…Another lipid mediator, 17HDoHE, which is a precursor to resolvins and possesses biological activity that inhibits TNF-a-induced IL-1b expression (37), was increased in lavage and lung homogenates after sEHI administration. Resolvins have been reported to promote the resolution of the allergic airways response (38).…”

Section: Discussionmentioning

confidence: 99%

Soluble Epoxide Hydrolase Inhibitor Attenuates Inflammation and Airway Hyperresponsiveness in Mice

Yang¹,

Bratt

Franzi

et al. 2015

Am J Respir Cell Mol Biol

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Control of airway inflammation is critical in asthma treatment. Soluble epoxide hydrolase (sEH) has recently been demonstrated as a novel therapeutic target for treating inflammation, including lung inflammation. We hypothesized that pharmacological inhibition of sEH can modulate the inflammatory response in a murine ovalbumin (OVA) model of asthma. BALB/c mice were sensitized and exposed to OVA over 6 weeks. A sEH inhibitor (sEHI) was administered for 2 weeks. Respiratory system compliance, resistance, and forced exhaled nitric oxide were measured. Lung lavage cell counts were performed, and selected cytokines and chemokines in the lung lavage fluid were measured. A LC/MS/MS method was used to measure 87 regulatory lipids mediators in plasma, lung tissue homogenates, and lung lavage fluid. The pharmacological inhibition of sEH increased concentrations of the antiinflammatory epoxy eicosatrienoic acids and simultaneously decreased the concentrations of the proinflammatory dihydroxyeicosatrienoic acids and dihydroxyoctadecenoic acids. All monitored inflammatory markers, including FeNO levels, and total cell and eosinophil numbers in the lung lavage of OVA-exposed mice were reduced by sEHI. The type 2 T helper cell (Th2) cytokines (IL-4, IL-5) and chemokines (Eotaxin and RANTES) were dramatically reduced after sEHI administration. Resistance and dynamic lung compliance were also improved by sEHI. We demonstrated that sEHI administration attenuates allergic airway inflammation and airway responsiveness in a murine model. sEHI may have potential as a novel therapeutic strategy for allergic asthma.Keywords: soluble epoxide hydrolase; asthma; inflammation; lipid mediators; type 2 T helper cell cytokines Clinical RelevanceWe demonstrated that inhibition of soluble epoxide hydrolase attenuates allergic airway inflammation and airway responsiveness in a murine model. Therefore, sEH inhibitors may have potential as a novel therapeutic strategy for allergic asthma.Three hundred million people worldwide suffer from episodic or persistent asthma (1). The cornerstones of treatment for persistent asthma are inhaled corticosteroids and b-agonist bronchodilators; however, a significant minority of patients with asthma does not respond well to these therapies (2). Thus, there are ongoing efforts to develop novel treatment strategies (3), such as specific antagonists of type 2 T helper cell (Th2) cytokines and mediators.

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“…11,13,21 We recently reported that AT-RvD1 inhibited acute cigarette smokee induced inflammation in mice, and accelerated resolution of inflammation after smoking cessation. 11 Here, we investigated whether AT-RvD1 inhibits the development of cigarette smokeeinduced airspace enlargement in a well-developed mouse model.…”

Section: At-rvd1 Inhibits Long-term Cigarette Smokeeinduced Airspace mentioning

confidence: 99%

Resolvin D1 Reduces Emphysema and Chronic Inflammation

Hsiao

Thatcher

Colas

et al. 2015

The American Journal of Pathology

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Chronic obstructive pulmonary disease is characterized, in part, by chronic inflammation that persists even after smoking cessation, suggesting that a failure to resolve inflammation plays an important role in the pathogenesis of the disease. It is widely recognized that the resolution of inflammation is an active process, governed by specialized proresolving lipid mediators, including lipoxins, resolvins, maresins, and protectins. Here, we report that proresolving signaling and metabolic pathways are disrupted in lung tissue from patients with chronic obstructive pulmonary disease, suggesting that supplementation with proresolving lipid mediators might reduce the development of emphysema by controlling chronic inflammation. Groups of mice were exposed long-term to cigarette smoke and treated with the proresolving mediator resolvin D1. Resolvin D1 was associated with a reduced development of cigarette smokeeinduced emphysema and airspace enlargement, with concurrent reductions in inflammation, oxidative stress, and cell death. Interestingly, resolvin D1 did not promote the differentiation of M2 macrophages and did not promote tissue fibrosis. Taken together, our results suggest that cigarette smoking disrupts endogenous proresolving pathways and that supplementation with specialized proresolving lipid mediators is an important therapeutic strategy in chronic lung disease, especially if endogenous specialized proresolving lipid mediator signaling is impaired. (Am J Pathol 2015, 185: 3189e3201; http:// dx.doi.org/10.1016/j.ajpath.2015 Chronic obstructive pulmonary disease (COPD) is a major global health problem and a leading cause of death and disability. Tobacco smoking remains the major causative factor in the development of COPD; however, new evidence suggests that household air pollution from fuel used for indoor cooking and heating is also a significant cause.

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Resolvin D1 and Aspirin-Triggered Resolvin D1 Promote Resolution of Allergic Airways Responses

Cited by 197 publications

References 43 publications

Inability to resolve specific infection generates innate immunodeficiency syndrome in Xiap−/− mice

Inability to resolve specific infection generates innate immunodeficiency syndrome in Xiap−/− mice

Soluble Epoxide Hydrolase Inhibitor Attenuates Inflammation and Airway Hyperresponsiveness in Mice

Resolvin D1 Reduces Emphysema and Chronic Inflammation

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