Neutrophil Resolvin E1 Receptor Expression and Function in Type 2 Diabetes

Freire, Marcelo; Dalli, Jesmond; Serhan, Charles N.; Dyke, Thomas E. Van

doi:10.4049/jimmunol.1601543

Cited by 73 publications

(83 citation statements)

References 56 publications

(52 reference statements)

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“…The expression levels of adhesive ligands and chemokine receptors were also reduced in inflammatory cells, subsequently suppressing inflammatory cell recruitment. Indeed, RvE1 has been shown to suppress neutrophil recruitment and promote phagocytosis-induced neutrophil apoptosis in various inflammation models, including carrageenaninduced paw inflammation, type 2 diabetes, and pulmonary inflammation (15,(52)(53)(54). Our data also showed that the inhibitory effects of RvE1 were mainly mediated by the BLT1 receptor, supporting previous research (15).…”

Section: Discussionsupporting

confidence: 90%

Resolvin E1 attenuates inj ury‐induced vascular neointimal formation by inhibition of inflammatory responses and vascular smooth muscle cell migration

et al. 2018

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Mechanical insults, such as stent implantation, can induce endothelial injury, vascular inflammation, and ultimately lead to vascular neointimal hyperplasia. Resolvin E1 (RvE1), derived from the ω3 fatty acid eicosapentaenoic acid, can facilitate the resolution of inflammation in many settings. We therefore aimed to determine if there was a role for RvE1 in preventing neointimal formation after arterial injury and to understand the underlying mechanisms. Vascular inflammation and neointimal hyperplasia were induced by wire injury in the femoral arteries of mice. Administration of exogenous RvE1 and endogenously generated RvE1 via dietary supplementation with eicosapentaenoic acid and aspirin markedly reduced vascular neointima formation in this model. Mechanistically, RvE1 was found to inhibit vascular neutrophil infiltration, promote macrophage polarization toward an M2-like phenotype, suppress T-cell trafficking by reducing RANTES secretion from vascular smooth muscle cells, and inhibit vascular smooth muscle cell migration. In summary, RvE1 demonstrated a protective role against vascular inflammation and remodeling in response to mechanical injury, suggesting that it may serve as an adjuvant therapeutic agent for percutaneous coronary interventions, such as stent implantation.-Liu, G., Gong, Y., Zhang, R., Piao, L., Li, X., Liu, Q., Yan, S., Shen, Y., Guo, S., Zhu, M., Yin, H., Funk, C. D., Zhang, J., Yu, Y. Resolvin E1 attenuates injury-induced vascular neointimal formation by inhibition of inflammatory responses and vascular smooth muscle cell migration.

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Section: Discussionsupporting

confidence: 90%

Resolvin E1 attenuates inj ury‐induced vascular neointimal formation by inhibition of inflammatory responses and vascular smooth muscle cell migration

et al. 2018

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“…Furthermore, RVE 1 does not only bind to the BLT 1 receptor but also binds to the ChemR23/ERV-1 receptor, which is expressed by neutrophils and mediates distinct biological effects than LTB 4 . 57 Given the structural similarities between 20-OH-LTB 4 and RVE 1 , (chemically a 18-OH-LTB 5 ), it remains possible that 20-OH-LTB 4 and 20-COOH-LTB 4 also bind to the ChemR23/ERV-1 receptor. To us, this is a primordial issue to be resolved, given the important levels of 20-OH-and 20-COOH-LTB 4 that have been documented in numerous biological samples.…”

Section: -Oh-ltb 4 and 20-cooh-ltbmentioning

confidence: 99%

20-Hydroxy- and 20-carboxy-leukotriene (LT) B4 downregulate LTB4-mediated responses of human neutrophils and eosinophils

Archambault

Poirier

Lefebvre

et al. 2019

Journal of Leukocyte Biology

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Leukotriene B4 (LTB4) plays a prominent role in innate immunity as it induces phagocyte recruitment, the release of antimicrobial effectors, and as it potentiates the ingestion and killing of pathogens. In humans, LTB4 has a short half‐life and is rapidly metabolized by leukocytes, notably into 20‐OH‐ and 20‐COOH‐LTB4 by neutrophils. Although these LTB4 metabolites bind to the BLT1 receptor with high affinity, they activate neutrophils to a much lower extent than LTB4. We thus postulated that LTB4 metabolites could dampen BLT1‐mediated responses, therefore limiting the impact of LTB4 on human neutrophil functions. We found that 20‐OH‐LTB4 and 20‐COOH‐LTB4 inhibited all of the LTB4‐mediated neutrophil responses we tested (migration, degranulation, leukotriene biosynthesis). The potencies of the different compounds at inhibiting LTB4‐mediated responses were 20‐OH‐LTB4 = CP 105,696 (BLT1 antagonist) > > 20‐COOH‐LTB4 ≥ resolvin E1 (RVE1). In contrast, the fMLP‐ and IL‐8‐mediated responses we tested were not affected by the LTB4 metabolites or RVE1. 20‐OH‐LTB4 and 20‐COOH‐LTB4 also inhibited the LTB4‐mediated migration of human eosinophils but not that induced by 5‐KETE. Moreover, using 20‐COOH‐LTB4, LTB4, and LTB4‐alkyne, we show that LTB4 is a chemotactic, rather than a chemokinetic factor for both human neutrophils and eosinophils. In conclusion, our data indicate that LTB4 metabolites and RVE1 act as natural inhibitors of LTB4‐mediated responses. Thus, preventing LTB4 ω‐oxidation might result in increased innate immunity and granulocyte functions.

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“…The resultant dysregulation of inflammation is central to phagocyte-mediated tissue injury in T2D and its periodontal complications. The return of inflamed tissues to health and homeostasis through active resolution of inflammation appears to be compromised in obesity and T2D (112). Omega 3 fatty acids and an increased omega-3/omega-6 ratio are associated with lower prevalence of coronary artery disease in Greenland Inuits and reduced incidence of diabetes in different populations (113).…”

Section: Pro-resolving Mediators Periodontitis and Systemic Diseasementioning

confidence: 99%

Pro-resolving mediators in the regulation of periodontal disease

Dyke¹

2017

Molecular Aspects of Medicine

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115

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Periodontitis is an inflammatory disease of the supporting structures of the dentition that is initiated by bacterial that form a biofilm on the surface of the teeth. The pathogenesis of the disease is a result of complex interactions between the biofilm and the host response that results in dysbiosis of the microbiome and dysregulation of the inflammatory response. Current data suggest that the excess inflammation associated with periodontitis is due to a failure of resolution of inflammation pathways. In this review, the relationship between inflammation and microbial dysbiosis is examined in the context of pro-inflammation and pro-resolution mediators and their ability to modify the course of disease. The impact of local oral inflammation on systemic inflammation and the relationship of periodontitis to other inflammatory diseases, including type 2 diabetes and cardiovascular disease is reviewed. Active resolvers of inflammation, including the lipoxins and resolvins, show great promise as therapeutics for the treatment of periodontitis and other inflammatory diseases.

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Neutrophil Resolvin E1 Receptor Expression and Function in Type 2 Diabetes

Cited by 73 publications

References 56 publications

Resolvin E1 attenuates inj ury‐induced vascular neointimal formation by inhibition of inflammatory responses and vascular smooth muscle cell migration

Resolvin E1 attenuates inj ury‐induced vascular neointimal formation by inhibition of inflammatory responses and vascular smooth muscle cell migration

20-Hydroxy- and 20-carboxy-leukotriene (LT) B4 downregulate LTB4-mediated responses of human neutrophils and eosinophils

Pro-resolving mediators in the regulation of periodontal disease

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