Not Only Glycaemic But Also Other Metabolic Factors Affect T Regulatory Cell Counts and Proinflammatory Cytokine Levels in Women with Type 1 Diabetes
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články
PubMed
28553653
PubMed Central
PMC5434466
DOI
10.1155/2017/5463273
Knihovny.cz E-zdroje
- MeSH
- cytokiny imunologie MeSH
- diabetes mellitus 1. typu komplikace farmakoterapie imunologie metabolismus MeSH
- diabetické neuropatie etiologie imunologie MeSH
- dospělí MeSH
- glykovaný hemoglobin metabolismus MeSH
- HDL-cholesterol metabolismus MeSH
- hypoglykemika aplikace a dávkování MeSH
- interleukin-1alfa imunologie MeSH
- interleukin-6 imunologie MeSH
- inzulin aplikace a dávkování MeSH
- LDL-cholesterol metabolismus MeSH
- lidé MeSH
- mladý dospělý MeSH
- počet lymfocytů MeSH
- produkty pokročilé glykace metabolismus MeSH
- regulační T-lymfocyty imunologie MeSH
- T-lymfocyty pomocné-indukující imunologie MeSH
- TNF-alfa imunologie MeSH
- triglyceridy metabolismus MeSH
- vitamin D metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mladý dospělý MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- cytokiny MeSH
- glykovaný hemoglobin MeSH
- HDL-cholesterol MeSH
- hemoglobin A1c protein, human MeSH Prohlížeč
- hypoglykemika MeSH
- IL1A protein, human MeSH Prohlížeč
- IL6 protein, human MeSH Prohlížeč
- interleukin-1alfa MeSH
- interleukin-6 MeSH
- inzulin MeSH
- LDL-cholesterol MeSH
- produkty pokročilé glykace MeSH
- TNF protein, human MeSH Prohlížeč
- TNF-alfa MeSH
- triglyceridy MeSH
- vitamin D MeSH
Type 1 diabetic (T1D) patients suffer from insulinopenia and hyperglycaemia. Studies have shown that if a patient's hyperglycaemic environment is not compensated, it leads to complex immune dysfunctions. Similarly, T1D mothers with poor glycaemic control exert a negative impact on the immune responses of their newborns. However, questions concerning the impact of other metabolic disturbances on the immune system of T1D mothers (and their newborns) have been raised. To address these questions, we examined 28 T1D women in reproductive age for the relationship between various metabolic, clinical, and immune parameters. Our study revealed several unexpected correlations which are indicative of a much more complex relationship between glucose and lipid factors (namely, glycosylated haemoglobin Hb1Ac, the presence of one but not multiple chronic diabetic complications, and atherogenic indexes) and proinflammatory cytokines (IL-1alpha and TNF-alpha). Regulatory T cell counts correlated with HbA1c, diabetic neuropathy, lipid spectra parameters, and IL-6 levels. Total T-helper cell count was interconnected with BMI and glycaemia variability correlated with lipid spectra parameters, insulin dose, and vitamin D levels. These and other correlations revealed in this study provide broader insight into the association of various metabolic abnormalities with immune parameters that may impact T1D mothers or their developing child.
Department of Physiology 2nd Medical Faculty Charles University Prague Czech Republic
Laboratory of Immunobiology Institute of Molecular Genetics of the ASCR Prague Czech Republic
Zobrazit více v PubMed
Atkinson M. A., Kaufman D. L., Campbell L., et al. Response of peripheral-blood mononuclear cells to glutamate decarboxylase in insulin-dependent diabetes. Lancet. 1992;339(8791):458–459. doi: 10.1016/0140-6736(92)91061-C. PubMed DOI
McDaniel C. F. Diabetes: a model of oxidative accelerated aging. Age (Omaha) 1999;22(4):145–148. doi: 10.1007/s11357-999-0016-1. PubMed DOI PMC
Polsky S., Ellis S. L. Obesity, insulin resistance, and type 1 diabetes mellitus. Current Opinion in Endocrinology, Diabetes, and Obesity. 2015;22(4):277–282. doi: 10.1097/MED.0000000000000170. PubMed DOI
Kurien M., Mollazadegan K., Sanders D. S., Ludvigsson J. F. Celiac disease increases risk of thyroid disease in patients with type 1 diabetes: a nationwide cohort study. Diabetes Care. 2016;39(3):371–375. doi: 10.2337/dc15-2117. PubMed DOI
Stechova K., Spalova I., Durilova M., et al. Influence of maternal hyperglycaemia on cord blood mononuclear cells in response to diabetes-associated autoantigens. Scandinavian Journal of Immunology. 2009;70(2):149–158. doi: 10.1111/j.1365-3083.2009.02282.x. PubMed DOI
Langley-Evans S. C. Nutrition in early life and the programming of adult disease: a review. Journal of Human Nutrition and Dietetics. 2015;28(Supplement 1):1–14. doi: 10.1111/jhn.12212. PubMed DOI
Santegoets S. J., Dijkgraaf E. M., Battaglia A., et al. Monitoring regulatory T cells in clinical samples: consensus on an essential marker set and gating strategy for regulatory T cell analysis by flow cytometry. Cancer Immunology, Immunotherapy. 2015;64(10):1271–1286. doi: 10.1007/s00262-015-1729-x. PubMed DOI PMC
Girgis C. M., Scalley B. D., Park K. E. Utility of the estimated glucose disposal rate as a marker of microvascular complications in young adults with type 1 diabetes. Diabetes Research and Clinical Practice. 2012;96(3):e70–e72. doi: 10.1016/j.diabres.2012.02.004. PubMed DOI
Varbo A., Benn M., Smith G. D., Timpson N. J., Tybjaerg-Hansen A., Nordestgaard B. G. Remnant cholesterol, low-density lipoprotein cholesterol, and blood pressure as mediators from obesity to ischemic heart disease. Circulation Research. 2015;116(4):665–673. doi: 10.1161/CIRCRESAHA.116.304846. PubMed DOI
Casqueiro J., Casqueiro J., Alves C. Infections in patients with diabetes mellitus: a review of pathogenesis. Indian Journal of Endocrinology and Metabolism. 2012;16(Supplement 1):S27–S36. doi: 10.4103/2230-8210.94253. PubMed DOI PMC
Newton R., Priyadharshini B., Turka L. A. Immunometabolism of regulatory T cells. Nature Immunology. 2016;17(6):618–625. doi: 10.1038/ni.3466. PubMed DOI PMC
Juarez D. T., Demaris K. M., Goo R., Mnatzaganian C. L., Wong Smith H. Significance of HbA1c and its measurement in the diagnosis of diabetes mellitus: US experience. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 2014;7:487–494. doi: 10.2147/DMSO.S39092. PubMed DOI PMC
El-Samahy M. H., Adly A. A., Ismail E. A., Salah N. Y. Regulatory T cells with CD62L or TNFR2 expression in young type 1 diabetic patients: relation to inflammation, glycemic control and micro-vascular complications. Journal of Diabetes and Its Complications. 2015;29(1):120–126. doi: 10.1016/j.jdiacomp.2014.07.004. PubMed DOI
Inchiostro S., Candido R., Cavalot F. How can we monitor glycaemic variability in the clinical setting? Diabetes, Obesity & Metabolism. 2013;15(Supplement 2):13–16. doi: 10.1111/dom.12142. PubMed DOI
Hayes C. E., Hubler S. L., Moore J. R., Barta L. E., Praska C. E., Nashold F. E. Vitamin D actions on CD4(+) T cells in autoimmune disease. Frontiers in Immunology. 2015;6:p. 100. doi: 10.3389/fimmu.2015.00100. PubMed DOI PMC
Al-Zubeidi H., Leon-Chi L., Newfield R. S. Low vitamin D level in pediatric patients with new onset type 1 diabetes is common, especially if in ketoacidosis. Pediatric Diabetes. 2016;17(8):592–598. doi: 10.1111/pedi.12342. PubMed DOI
Strange R. C., Shipman K. E., Ramachandran S. Metabolic syndrome: a review of the role of vitamin D in mediating susceptibility and outcome. World Journal of Diabetes. 2015;6(7):896–911. doi: 10.4239/wjd.v6.i7.896. PubMed DOI PMC
Thomas G. N., Scragg R., Jiang C. Q., et al. Hyperglycaemia and vitamin D: a systematic overview. Current Diabetes Reviews. 2012;8(1):18–31. doi: 10.2174/157339912798829223. PubMed DOI
Dinarello C. A. Immunological and inflammatory functions of the interleukin-1 family. Annual Review of Immunology. 2009;27:519–550. doi: 10.1146/annurev.immunol.021908.132612. PubMed DOI
Nazir N., Siddiqui K., Al-Qasim S., Al-Naqeb D. Meta-analysis of diabetic nephropathy associated genetic variants in inflammation and angiogenesis involved in different biochemical pathways. BMC Medical Genetics. 2014;15(1):p. 103. doi: 10.1186/s12881-014-0103-8. PubMed DOI PMC
Bour-Jordan H., Thompson H. L., Giampaolo J. R., Davini D., Rosenthal W., Bluestone J. A. Distinct genetic control of autoimmune neuropathy and diabetes in the non-obese diabetic background. Journal of Autoimmunity. 2013;45:58–67. doi: 10.1016/j.jaut.2013.06.005. PubMed DOI PMC
Ziegler S. F., Buckner J. H. FOXP3 and the regulation of Treg/Th17 differentiation. Microbes and Infection. 2009;11(5):594–598. doi: 10.1016/j.micinf.2009.04.002. PubMed DOI PMC
Vcelakova J., Blatny R., Halbhuber Z., et al. The effect of diabetes-associated autoantigens on cell processes in human PBMCs and their relevance to autoimmune diabetes development. Journal of Diabetes Research. 2013;2013:p. 10. doi: 10.1155/2013/589451.589451 PubMed DOI PMC
Reinert-Hartwall L., Honkanen J., Salo H. M., et al. Th1/Th17 plasticity is a marker of advanced β cell autoimmunity and impaired glucose tolerance in humans. Journal of Immunology. 2015;194(1):68–75. doi: 10.4049/jimmunol.1401653. PubMed DOI PMC
Cucak H., Vistisen D., Witte D., Philipsen A., Rosendahl A. Reduction of specific circulating lymphocyte populations with metabolic risk factors in patients at risk to develop type 2 diabetes. PLoS One. 2014;9(9, article e107140) doi: 10.1371/journal.pone.0107140. PubMed DOI PMC
Zeng C., Shi X., Zhang B., et al. The imbalance of Th17/Th1/Tregs in patients with type 2 diabetes: relationship with metabolic factors and complications. Journal of Molecular Medicine (Berlin, Germany) 2012;90(2):175–186. doi: 10.1007/s00109-011-0816-5. PubMed DOI
Wilhelm A. J., Zabalawi M., Owen J. S., et al. Apolipoprotein A-I modulates regulatory T cells in autoimmune LDLr−/−, ApoA-I−/− mice. The Journal of Biological Chemistry. 2010;285(46):36158–36169. doi: 10.1074/jbc.M110.134130. PubMed DOI PMC
Katoh H., Zheng P., Liu Y. FOXP3: genetic and epigenetic implications for autoimmunity. Journal of Autoimmunity. 2013;41:72–78. doi: 10.1016/j.jaut.2012.12.004. PubMed DOI PMC
Otsubo K., Kanegane H., Kamachi Y., et al. Identification of FOXP3-negative regulatory T-like (CD4(+)CD25(+)CD127(low)) cells in patients with immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome. Clinical Immunology. 2011;141(1):111–120. doi: 10.1016/j.clim.2011.06.006. PubMed DOI