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      A specific combined long-chain polyunsaturated fatty acid supplementation reverses fatty acid profile alterations in a mouse model of chronic asthma

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          Abstract

          Background

          The immune-modulating potential of long-chain polyunsaturated fatty acids (LCPUFAs) based on their conversion into lipid mediators in inflammatory situations has been proven by several studies. Respecting the immune-modulative role of lipid mediators in bronchoconstriction, airway inflammation and resolution of inflammatory processes, LCPUFAs play an important role in asthma. To design a disease-specific and most beneficial LCPUFA supplementation strategy, it is essential to understand how asthma alters LCPUFA profiles. Therefore, this study characterizes the alterations of LCPUFA profiles induced by allergic asthma. In addition, this study explores whether a simple eicosapentaenoic acid (EPA) alone or a specific combined LCPUFA supplementation could restore imbalanced LCPUFA profiles.

          Methods

          Mice were sensitized with a daily dose of 40 μg house dust mite (HDM)-extract in a recall model and fed with either normal diet, EPA or a specific combined (sc)-LCPUFA supplementation containing EPA, docosahexaenoic acid (DHA), γ -linolenic acid (GLA) and stearidonic acid (SDA) for 24 days. After recall with HDM, mice were sacrificed and blood and lung tissue were collected. Fatty acid profiles were determined in plasma, blood cells and lung cells of asthmatic mice by capillary gas-chromatography.

          Results

          In lung cells of asthmatic mice, arachidonic acid (AA, p < 0.001) and DHA ( p < 0.01) were increased while dihomo-γ-linolenic acid (DGLA, p < 0.05) was decreased. EPA supplementation increased only EPA ( p < 0.001) and docosapentaenoic acid (DPA, p < 0.001), but neither DGLA nor DHA in lung cells of asthmatic mice. In contrast, a specific combined dietary supplementation containing n-3 and n-6 LCPUFAs could decrease AA ( p < 0.001), increase EPA ( p < 0.001), DPA ( p < 0.001) and DHA ( p < 0.01) and could reverse the lack of DGLA ( p < 0.05).

          Conclusions

          In summary, allergic asthma alters LCPUFA profiles in blood and lung tissue. In contrast to the EPA supplementation, the distinct combination of n-3 and n-6 LCPUFAs restored the LCPUFA profiles in lung tissue of asthmatic mice completely. Subsequently, sc-LCPUFA supplementation is likely to be highly supportive in limiting and resolving the inflammatory process in asthma.

          Electronic supplementary material

          The online version of this article (10.1186/s12944-018-0947-6) contains supplementary material, which is available to authorized users.

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          Most cited references19

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          Innate and adaptive immune responses in asthma.

          The recognition that asthma is primarily an inflammatory disorder of the airways associated with T helper type 2 (T(H)2) cell-dependent promotion of IgE production and recruitment of mast cells and eosinophils has provided the rationale for disease control using inhaled corticosteroids and other anti-inflammatory drugs. As more has been discovered about the cytokine, chemokine and inflammatory pathways that are associated with T(H)2-driven adaptive immunity, attempts have been made to selectively inhibit these in the hope of discovering new therapeutics as predicted from animal models of allergic inflammation. The limited success of this approach, together with the recognition that asthma is more than allergic inflammation, has drawn attention to the innate immune response in this disease. Recent advances in our understanding of the sentinel role played by innate immunity provides new targets for disease prevention and treatment. These include pathways of innate stimulation by environmental or endogenous pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) to influence the activation and trafficking of DCs, innate sources of cytokines, and the identification of new T cell subsets and lymphoid cells.
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            Specialized pro-resolving mediators: endogenous regulators of infection and inflammation

            Key Points The immune response comprises not only pro-inflammatory and anti-inflammatory pathways but also pro-resolution mechanisms that serve to balance the need of the host to target microbial pathogens while preventing excess inflammation and bystander tissue damage. Specialized pro-resolving mediators (SPMs) are enzymatically derived from essential fatty acids to serve as a novel class of immunoresolvents that limit acute responses and orchestrate the clearance of tissue pathogens, dying cells and debris from the battlefield of infectious inflammation. SPMs are composed of lipoxins, E-series and D-series resolvins, protectins and maresins. Individual members of the SPM family serve as agonists at cognate receptors to induce cell-type specific responses. Important regulatory roles for SPMs have been uncovered in host responses to several microorganisms, including bacterial, viral, fungal and parasitic pathogens. SPMs also promote the resolution of non-infectious inflammation and tissue injury. Defects in host SPM pathways contribute to the development of chronic inflammatory diseases. With the capacity to enhance host defence and modulate inflammation, SPMs represent a promising translational approach to enlist host resolution programmes for the treatment of infection and excess inflammation. Supplementary information The online version of this article (doi:10.1038/nri.2015.4) contains supplementary material, which is available to authorized users.
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              The resolution code of acute inflammation: Novel pro-resolving lipid mediators in resolution.

              Studies into the mechanisms in resolution of self-limited inflammation and acute reperfusion injury have uncovered a new genus of pro-resolving lipid mediators coined specialized pro-resolving mediators (SPM) including lipoxins, resolvins, protectins and maresins that are each temporally produced by resolving-exudates with distinct actions for return to homeostasis. SPM evoke potent anti-inflammatory and novel pro-resolving mechanisms as well as enhance microbial clearance. While born in inflammation-resolution, SPM are conserved structures with functions discovered in microbial defense, pain, organ protection and tissue regeneration, wound healing, cancer, reproduction, and neurobiology-cognition. This review covers these SPM mechanisms and other new omega-3 PUFA pathways that open their path for functions in resolution physiology.
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                Author and article information

                Contributors
                +49(0)69-6301 85644 , daniela.fussbroich@lt.hs-fulda.de
                Journal
                Lipids Health Dis
                Lipids Health Dis
                Lipids in Health and Disease
                BioMed Central (London )
                1476-511X
                18 January 2019
                18 January 2019
                2019
                : 18
                : 16
                Affiliations
                [1 ]GRID grid.430588.2, Department of Food Technology, , University of Applied Science Fulda, ; Leipziger Str. 123, 36039 Fulda, Germany
                [2 ]ISNI 0000 0004 1936 9721, GRID grid.7839.5, Division for Allergy, Pneumology and Cystic Fibrosis, Department for Children and Adolescence, , Goethe University, ; Theodor-Stern-Kai 7, Frankfurt/Main, Germany
                [3 ]ISNI 0000 0004 1936 9721, GRID grid.7839.5, Faculty of Biological Sciences, , Goethe University, ; Max-von-Laue-Straße 13, Frankfurt/Main, Germany
                Author information
                http://orcid.org/0000-0003-4503-8574
                Article
                947
                10.1186/s12944-018-0947-6
                6339374
                30658644
                f30983f2-33a8-4048-86f1-a1361ce97325
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 27 April 2018
                : 17 December 2018
                Categories
                Research
                Custom metadata
                © The Author(s) 2019

                Biochemistry
                omega-3,omega-6,lcpufa,asthma,fatty acid profiles,gas-chromatography
                Biochemistry
                omega-3, omega-6, lcpufa, asthma, fatty acid profiles, gas-chromatography

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