Department of Food Technology, University of Applied Science Fulda, Leipziger Str. 123, 36039, Fulda, Germany.
Division for Allergy, Pneumology and Cystic Fibrosis, Department for Children and Adolescence, Goethe University, Theodor-Stern-Kai 7, Frankfurt/Main, Germany.
Lipids Health Dis. 2019 Jan 18;18(1):16. doi: 10.1186/s12944-018-0947-6.
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.
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.
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).
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.
长链多不饱和脂肪酸(LCPUFAs)基于其在炎症情况下转化为脂质介质的免疫调节潜力,已被多项研究证明。鉴于脂质介质在支气管收缩、气道炎症和炎症过程消退中的免疫调节作用,LCPUFAs 在哮喘中发挥着重要作用。为了设计针对特定疾病且最有益的 LCPUFA 补充策略,了解哮喘如何改变 LCPUFA 谱至关重要。因此,本研究描述了过敏性哮喘引起的 LCPUFA 谱改变。此外,本研究还探讨了单纯的二十碳五烯酸(EPA)补充或特定的联合 LCPUFA 补充是否可以恢复失衡的 LCPUFA 谱。
在回忆模型中,用每日 40μg 屋尘螨(HDM)提取物对小鼠进行致敏,并分别用普通饮食、EPA 或特定的联合(sc)-LCPUFA 补充剂(含 EPA、二十二碳六烯酸(DHA)、γ-亚麻酸(GLA)和硬脂酸(SDA))喂养 24 天。用 HDM 进行回忆后,处死小鼠并收集血液和肺组织。通过毛细管气相色谱法测定哮喘小鼠血浆、血细胞和肺细胞中的脂肪酸谱。
在哮喘小鼠的肺细胞中,花生四烯酸(AA,p<0.001)和 DHA(p<0.01)增加,而二同型-γ-亚麻酸(DGLA,p<0.05)减少。EPA 补充仅增加 EPA(p<0.001)和二十二碳五烯酸(DPA,p<0.001),但不增加哮喘小鼠肺细胞中的 DGLA 或 DHA。相比之下,含 n-3 和 n-6 LCPUFAs 的特定联合饮食补充可以降低 AA(p<0.001),增加 EPA(p<0.001)、DPA(p<0.001)和 DHA(p<0.01),并逆转 DGLA 缺乏(p<0.05)。
总之,过敏性哮喘改变了血液和肺组织中的 LCPUFA 谱。与 EPA 补充不同,n-3 和 n-6 LCPUFA 的特定组合完全恢复了哮喘小鼠肺组织中的 LCPUFA 谱。随后,sc-LCPUFA 补充可能非常有助于限制和解决哮喘中的炎症过程。