Shifts in the immunoepigenomic landscape of monocytes in response to a diabetes-specific social support intervention: a pilot study among Native Hawaiian adults with diabetes.
Shifts in the immunoepigenomic landscape of monocytes in response to a diabetes-specific social support intervention: a pilot study among Native Hawaiian adults with diabetes.
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DOI：
10.1186/s13148-022-01307-6
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发表时间：
2022-07-18
影响因子：
5.7
通讯作者：
中科院分区：
文献类型：
--
作者：
夏威夷原住民尤其容易受到 2 型糖尿病 (DM) 的影响，这是一种以高血糖和全身炎症为特征的慢性代谢性非传染性疾病。持续不断的全身炎症常常会导致一系列与糖尿病相关的合并症，包括心血管疾病、微血管并发症和肾功能障碍。然而，很少有研究探讨细胞水平上的慢性炎症与其与标准糖尿病治疗（例如糖尿病特异性生活方式和社会支持教育）之间的关系，而这些治疗被公认为糖尿病护理临床标准的基石。这项试点研究的目的是在患有 DM 的高危夏威夷原住民成人中实施为期 3 个月的糖尿病特定社会支持计划后，利用表观遗传学、免疫学和临床措施探索单核细胞炎症的关联。从 16 名患有 DM 的夏威夷原住民成年人样本中，随机选择 8 名个体的外周血单核细胞 (PBMC) 富集的单核细胞进行表观基因组分析。使用 Illumina HumanMmethylation450 BeadChip 微阵列，在基线和 DM 特定社会支持计划 (DM-SSP) 后 3 个月的参与者单核细胞中鉴定出 1,061 个差异甲基化位点 (DML)。基因本体分析表明，这些 DML 富含参与免疫、代谢和心脏代谢途径的基因，其中一部分也存在显着差异表达。免疫功能的离体分析显示，DM-SSP 后与基线相比有所改善，其特征是单核细胞的白细胞介素 1β 和 IL-6 分泌减弱。 DM-SSP 响应的细胞因子分泌改变与干预时间点之间单核细胞中免疫相关基因的甲基化和基因表达状态的变化显着相关。我们的试点研究提供了炎症单核细胞活性变化的初步证据，这些变化可能是由表观遗传修饰驱动的，在 DM 特异性 SSP 干预后 3 个月。这些单核细胞炎症状态轨迹的新变化是在患有 DM 的高危夏威夷原住民中调节免疫和代谢基因转录的位点上发现的，这表明心理社会行为的改善与糖尿病特异性 SSP 后免疫表观遗传模式的变化之间存在关系。需要进一步的研究来调查社会支持如何通过慢性炎症性疾病（如糖尿病）的免疫表观遗传修饰影响全身炎症。 在线版本包含可在 10.1186/s13148-022-01307-6 获取的补充材料。
Native Hawaiians are disproportionately affected by type 2 diabetes mellitus (DM), a chronic metabolic, non-communicable disease characterized by hyperglycemia and systemic inflammation. Unrelenting systemic inflammation frequently leads to a cascade of multiple comorbidities associated with DM, including cardiovascular disease, microvascular complications, and renal dysfunction. Yet few studies have examined the link between chronic inflammation at a cellular level and its relationship to standard DM therapies such as diabetes-specific lifestyle and social support education, well recognized as the cornerstone of clinical standards of diabetes care. This pilot study was initiated to explore the association of monocyte inflammation using epigenetic, immunologic, and clinical measures following a 3-month diabetes-specific social support program among high-risk Native Hawaiian adults with DM. From a sample of 16 Native Hawaiian adults with DM, monocytes enriched from peripheral blood mononuclear cells (PBMCs) of 8 individuals were randomly selected for epigenomic analysis. Using the Illumina HumanMethylation450 BeadChip microarray, 1,061 differentially methylated loci (DML) were identified in monocytes of participants at baseline and 3 months following a DM-specific social support program (DM-SSP). Gene ontology analysis showed that these DML were enriched within genes involved in immune, metabolic, and cardiometabolic pathways, a subset of which were also significantly differentially expressed. Ex vivo analysis of immune function showed improvement post-DM-SSP compared with baseline, characterized by attenuated interleukin 1β and IL-6 secretion from monocytes. Altered cytokine secretion in response to the DM-SSP was significantly associated with changes in the methylation and gene expression states of immune-related genes in monocytes between intervention time points. Our pilot study provides preliminary evidence of changes to inflammatory monocyte activity, potentially driven by epigenetic modifications, 3 months following a DM-specific SSP intervention. These novel alterations in the trajectory of monocyte inflammatory states were identified at loci that regulate transcription of immune and metabolic genes in high-risk Native Hawaiians with DM, suggesting a relationship between improvements in psychosocial behaviors and shifts in the immunoepigenetic patterns following a diabetes-specific SSP. Further research is warranted to investigate how social support influences systemic inflammation via immunoepigenetic modifications in chronic inflammatory diseases such as DM. The online version contains supplementary material available at 10.1186/s13148-022-01307-6.
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影响因子：
16.2
作者：
De Rekeneire, Nathalie;Kritchevsky, Stephen B.;Harris, Tamara B.
通讯作者：
Harris, Tamara B.
影响因子：
3.7
作者：
Li D;Le Pape MA;Parikh NI;Chen WX;Dye TD
通讯作者：
Dye TD
影响因子：
2.9
作者：
Pinzón-Cortés JA;Perna-Chaux A;Rojas-Villamizar NS;Díaz-Basabe A;Polanía-Villanueva DC;Jácome MF;Mendivil CO;Groot H;López-Segura V
通讯作者：
López-Segura V
DOI：
10.1161/atvbaha.118.312135
发表时间：
2019-04-01
影响因子：
8.7
作者：
Davis, Frank M.;Gallagher, Katherine A.
通讯作者：
Gallagher, Katherine A.
影响因子：
4.6
作者：
Corley MJ;Dye C;D'Antoni ML;Byron MM;Yo KL;Lum-Jones A;Nakamoto B;Valcour V;SahBandar I;Shikuma CM;Ndhlovu LC;Maunakea AK
通讯作者：
Maunakea AK