Dysregulated synthesis of protectin D1 in eosinophils from patients with severe asthma

Miyata, Jun; Fukunaga, Koichi; Iwamoto, Ryo; Isobe, Yosuke; Niimi, Kyoko; Takamiya, Rina; Takihara, Takahisa; Tomomatsu, Katsuyoshi; Suzuki, Yuzo; Oguma, Tsuyoshi; Sayama, Koichi; Arai, Hiroyuki; Betsuyaku, Tomoko; Arita, Makoto; Asano, Koichiro

doi:10.1016/j.jaci.2012.07.048

Cited by 112 publications

(95 citation statements)

References 45 publications

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“…Higher urinary ATL levels in aspirin-tolerant asthma than in aspirin-intolerant asthma (Sanak et al 2000;Levy et al 2005;Yamaguchi et al 2011) and regulate natural killer (NK) cell and innate lymphoid cell activation (Barnig et al 2013;Peebles 2013) Alzheimer's disease (AD) LXA 4 levels are reduced in AD brain and CSF RvD1 and RvD2 identified in human adipocytes from obese patients (Clària et al 2012) Human plasma and milk RvE1 identified in human plasma (Psychogios et al 2011) and milk (Weiss et al 2013) Multiple sclerosis RvD1 was detected and up-regulated in serum and cerebrospinal fluid in the highly active group (Pruss et al 2013) Human IgA nephropathy RvE1 identified in patients supplemented with fish oil n-3 (Zivkovic et al 2012) Protectin Asthma PD1 in exhaled breath condensates in asthma exacerbation (Levy et al 2007); decreased PD1 in eosinophils from patients with severe asthma compared with healthy individuals (Miyata et al 2013) Embryonic stem cells PD1 produced in embryonic stem cells (Yanes et al 2010) Multiple sclerosis NPD1 was detected in serum and cerebrospinal fluid in the highly active group (Pruss et al 2013) Maresins Synovial fluid MaR1 identified in synovial fluid from arthritis patients (Giera et al 2012) han et al Morris et al 2009;Wu et al 2009Wu et al , 2013. Recently, the stereochemical structures of resolvin D1 (RvD1; 7S,8R,17S-trihydroxy-4Z, 9E,11E,13Z,15E,19Z-docosahexaenoic acid), its AT 17R-epimer ), RvD2 (resolvin D2, 7S,16R,17S-trihydroxy-4Z, 8E,10Z, 12E,14E,19Z-docosahexaenoic acid) ), AT-protectin D1 (PD1; protectin D1/neuroprotectin D1, 10R,17S-dihydroxy-4Z, 7Z,11E,13E,15Z,19Z-docosahexaenoic acid) , and maresin 1 (MaR1; maresin 1, 7R,14S-dihydroxy-docosa-4Z,8E, 10E, 12Z,16Z,19Z-hexaenoic acid) were each assigned, as well as their biosynthetic-related isomers, and several made commercially available.…”

Section: Asthmamentioning

confidence: 99%

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Lipid Mediators in the Resolution of Inflammation

Serhan

Chiang

Dalli

et al. 2014

Cold Spring Harb Perspect Biol

432

350

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Mounting of the acute inflammatory response is crucial for host defense and pivotal to the development of chronic inflammation, fibrosis, or abscess formation versus the protective response and the need of the host tissues to return to homeostasis. Within self-limited acute inflammatory exudates, novel families of lipid mediators are identified, named resolvins (Rv), protectins, and maresins, which actively stimulate cardinal signs of resolution, namely, cessation of leukocytic infiltration, counterregulation of proinflammatory mediators, and the uptake of apoptotic neutrophils and cellular debris. The biosynthesis of these resolution-phase mediators in sensu stricto is initiated during lipid-mediator class switching, in which the classic initiators of acute inflammation, prostaglandins and leukotrienes (LTs), switch to produce specialized proresolving mediators (SPMs). In this work, we review recent evidence on the structure and functional roles of these novel lipid mediators of resolution. Together, these show that leukocyte trafficking and temporal spatial signals govern the resolution of self-limited inflammation and stimulate homeostasis.

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Section: Asthmamentioning

confidence: 99%

“…PD1, in nanomolar concentrations, reduces eosinophil chemotaxis and adhesion molecules (Miyata et al 2013). In cigarette smoke-induced lung inflammation in the airways of mice, RvD1 protects and reduces PMN infiltration.…”

Section: New Uses Of Spms In Animal Disease Modelsmentioning

confidence: 99%

Lipid Mediators in the Resolution of Inflammation

Serhan

Chiang

Dalli

et al. 2014

Cold Spring Harb Perspect Biol

432

350

View full text Add to dashboard Cite

show abstract

“…However, the SPMs are likely to be important in a number of human conditions associated with infl ammation. In this respect, biosynthesis of protectin D1 by eosinophils is reduced in patients with severe asthma ( 12 ). MaR-1 has been identifi ed in synovial fl uid of patients with rheumatoid arthritis ( 13 ) and RvD1 and RvD2 have been identifi ed in adipose tissue of healthy patients, whereas PD1 and 17-HDHA are reduced in subcutaneous adipose tissue of patients with peripheral artery disease ( 14 ).…”

Section: Separation Of Spms Using Reverse Phase Lc/ms/msmentioning

confidence: 99%

Short-term n-3 fatty acid supplementation but not aspirin increases plasma proresolving mediators of inflammation

Barden

Mas

Croft

et al. 2014

Journal of Lipid Research

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the infl ammatory process ( 1, 2 ), acting on a number of G-coupled protein receptors, including the leukotriene B4 (LTB 4 ) receptor to affect resolution of infl ammation.Metabolism of EPA by acetylated cyclooxygenase (COX)-2 or cytochrome P450 monooxygenase results in the formation of 18-hydroxyeicosapentaenoic acid (18-HEPE) that can be converted by 5-lipoxygenase (LOX) to 5-hydroperoxy-18-hydroxyeicosapentaenoic acid (5-Hp-18-HEPE). The latter can undergo epoxidation and enzyme hydrolysis to yield resolvin E1 (RvE1), or reduction to yield resolvin E2 (RvE2). A third E-series resolvin, resolvin E3 (RvE3), is generated from EPA by the 12/15 LOX pathway ( 3 ). Studies using chiral chromatography indicate that acetylation of COX-2 by aspirin generates both 18S-HEPE and 18R-HEPE and their respective downstream E-series resolvins 18S-RvE1 and 18R-RvE1 ( 4 ).Metabolism of DHA by either acetylated COX-2 or 15-LOX gives rise to 17-hydroperoxydocosahexaenoic acid (17-HpDHA) that is converted to 17-hydroxydocosahexaenoic acid (17-HDHA). 15-LOX gives rise to mainly 17S-HpDHA whereas acetylated COX-2 yields 17R-HpDHA ( 5 ). The action of 5-LOX on 17-HDHA generates the Dseries resolvins RvD1-RvD6 ( 1 ). In the absence of 5-LOX, protectin D1 (PD1) is formed from 17-HpDHA. In macrophages, 12/15-LOX can act on DHA to form 14-hydroperoxydocosahexaenoic acid (14-HpDHA) that can be further metabolized to 14-hydroxydocosahexaenoic acid (14-HDHA) and the maresins ( 6 ).Most of the research on the effects of SPMs has been in animal models. The resolvins and protectins have been Abstract Resolution of infl ammation is an active process involving specialized proresolving mediators (SPM) formed from the n-3 fatty acids. This study examined the effect of n-3 fatty acid supplementation and aspirin on plasma SPMs in healthy humans. Healthy volunteers (n = 21) were supplemented with n-3 fatty acids (2.4g/day) for 7 days with random assignment to take aspirin (300 mg/day) or placebo from day 5 to day 7. Blood was collected at baseline (day 0 There is increasing interest in the role of the specialized proresolving mediators (SPMs) that actively stimulate resolution of infl ammation ( 1 ). In particular, recent attention has focused on those SPM derived from the long-chain n-3 fatty acids EPA and DHA. The SPMs formed from EPA are known as E-series resolvins, while those formed from DHA include protectins, D-series resolvins, and maresins ( 1 ). Studies have shown that SPMs increase with time during A.B., T.A.M.,)

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“…Recently, it was discovered that omega-3-derived SPMs are key mediators that possess proresolving activities (22). Evidence supports the hypothesis that asthma represents, at least in part, a failure to resolve chronic inflammation, with an imbalance between proinflammatory and proresolving mediators (23)(24)(25)(26)(27). For example, severe asthma patients have lower levels of LxA 4 in BAL fluid and in exhaled breath condensate compared with patients with mild asthma (24,25).…”

Section: Discussionmentioning

confidence: 94%