ISSN 2415-3060 (print), ISSN 2522-4972 (online)
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JMBS 2019, 4(4): 72–76
https://doi.org/10.26693/jmbs04.04.072
Clinical Medicine

Changes of the Citokinate Status Parameters on the Basis of Determination of Activity of Calprotectin and Interleukin-22 in Patients with Acute Myocardial Infarction with Diabetes Mellitus Type 2

Zhuravlova M., Ryndina N., Kravchun P.
Abstract

The purpose of the study was to evaluate changes in the pro-and anti-inflammatory parameters of the cytokine status based on the determination of the activity of calprotectin and interleukin-22 in patients with acute myocardial infarction, depending on the presence or absence of concomitant type 2 diabetes, as well as to analyze the relationships between cytokinemia and carbohydrate metabolism in the studied cohorts of patients. Material and methods. A total of 110 patients (mean age 65.25±0.09 years) who were on treatment in the infarctional department of Kharkiv city clinical hospital №27 and Kharkiv clinical hospital on railway transport №1 were examined. 64 patients (average age 65, 31±1.62 years) for acute myocardial infarction with concomitant type 2 diabetes mellitus. The comparison group was 46 patients with isolated acute myocardial infarction (mean age 65.19±1.22 years). Results and discussion. Blood glucose concentration was determined by glucose oxidase method. Determination of the level of insulin was carried out using the immunoassay method using the test system EIA-2935, Insulin ELISA. Determination of serum calprotectin level was performed by immunoassay using the MRP8 / 14 ELISA KIT test system. Determination of the level of interleukin-22 serum was carried out by immunoassay using the human IL-22 ELISA KIT test system. Conclusions. The resulting linkages between calprotectin and IL-22 in patients with isolated acute myocardial infarction indicate a high activity both pro- and anti-inflammatory levels of cytokine status. In patients with acute myocardial infarction type 2, the hyperactivity of the proinflammatory indicator of calprotectin was associated with a decrease in anti-inflammatory IL-22, which proved that there was no compensatory reaction in this cohort of patients.

Keywords: diabetes mellitus type 2, acute myocardial infarction, interleukin-22, serum calprotectin

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References
  1. Townsend N, Wilson L, Bhatnagar P, Wickramasinghe K, Rayner M, Nichols M. Cardiovascular disease in Europe: epidemiological update 2016. Eur Heart J. 2016; 37(42): 3232-45. https://www.ncbi.nlm.nih.gov/pubmed/27523477. https://doi.org/10.1093/eurheartj/ehw334
  2. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. ESC Scientific Document Group 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). European Heart Journal. 2018; 39(2): 119-77. https://www.ncbi.nlm.nih.gov/pubmed/28886621. https://doi.org/10.1093/eurheartj/ehx393
  3. Hartley A, Marshall DC, Salciccioli JD, Sikkel MB, Maruthappu M, Shalhoub J. Trends in mortality from ischemic heart disease and cerebrovascular disease in Europe: 1980 to 2009. Circulation. 2016; 133(20): 1916-26. https://www.ncbi.nlm.nih.gov/pubmed/27006480. https://doi.org/10.1161/CIRCULATIONAHA.115.018931
  4. Striz I & Trebichavsky I. Calprotectin – a pleiotropic molecule in acute and chronic inflammation. Physiological Research. 2004; 53(3): 245–53. https://www.ncbi.nlm.nih.gov/pubmed/15209531
  5. Manitz MP, Horst B, Seeliger S, Strey A, Skryabin BV, Gunzer M, et al. Loss of S100A9 (MRP14) results in reduced interleukin-8-induced CD11b surface expression, a polarized microfilament system, and diminished responsiveness to chemoattractants in vitro. Molecular and Cellular Biology. 2003; 23(3): 1034–43. https://www.ncbi.nlm.nih.gov/pubmed/12529407. https://www.ncbi.nlm.nih.gov/pmc/articles/140712. https://doi.org/10.1128/MCB.23.3. 1034-1043.2003
  6. Wolk K, Witte E, Witte K, Warszawska K, Sabat R. Biology of interleukin-22. Seminars in Immunopathology. 2010; 32(1): 17–31. https://www.ncbi.nlm.nih.gov/pubmed/20127093. https://doi.org/10.1007/s00281-009-0188-x
  7. Lin YZ, Wu BW, Lu ZD, Huang Y, Shi Y, Liu H, et al. Circulating Th22 and Th9 Levels in Patients with Acute Coronary Syndrome. Mediators of Inflammation. 2013; 2013: 635672. https://www.ncbi.nlm.nih.gov/pubmed/24453425. https://www.ncbi.nlm.nih.gov/pmc/articles/3884785. https://doi.org/10.1155/2013/635672
  8. Dalmas E, Venteclef N, Caer C, Poitou C, Cremer I, Aron-Wisnewsky J, et al. T cell+derived IL-22 amplifies IL-1β+driven inflammation in human adipose tissue: relevance to obesity and type 2 diabetes. Diabetes. 2014; 63(6): 1966–77. https://www.ncbi.nlm.nih.gov/pubmed/24520123. https://doi.org/10.2337/db13-1511
  9. Wang X, Ota N, Manzanillo P, Kates L, Zavala-Solorio J, Eidenschenk C, et al. Interleukin-22 alleviates metabolic disorders and restores mucosal immunity in diabetes. Nature. 2014; 514(7521): 237–41. https://www.ncbi.nlm.nih.gov/pubmed/25119041. https://doi.org/10.1038/nature13564
  10. Gong F, Wu J, Zhou P, Zhang M, Liu J, Liu Y, et al. Interleukin-22 Might Act as a Double-Edged Sword in Type 2 Diabetes and Coronary Artery Disease. Mediators Inflamm. 2016; 2016: 8254797. https://www.ncbi.nlm.nih.gov/pubmed/27829708. https://www.ncbi.nlm.nih.gov/pmc/articles/5088317. https://doi.org/10.1155/2016/8254797
  11. Paneni F, Beckman JA, Creager MA, Cosentino F. Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I. European Heart Journal. 2013; 34(31): 2436–46. https://www.ncbi.nlm.nih.gov/pubmed/23641007. https://www.ncbi.nlm.nih.gov/pmc/articles/3743069. https://doi.org/10.1093/eurheartj/eht149
  12. Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk. Arteriosclerosis, Thrombosis, and Vascular Biology. 2003; 23(2): 168–75. https://www.ncbi.nlm.nih.gov/pubmed/12588755. https://doi.org/10.1161/01.atv.0000051384.43104.fc