Polymorphism of protein genes associated with endothelial function in patients with infective endocarditis
https://doi.org/10.15829/1560-4071-2018-10-88-97
Abstract
Aim. To study relationship between the polymorphism of five polymorphic sites of EDN1, SELE, SELP, SELPLG genes with the risk of infectious endocarditis (IE) and the connection of genotypes of studied sites with concentration of the corresponding proteins in the blood.
Material and methods. The study included 208 patients with IE and 300 healthy donors. Genotyping was performed on 6 polymorphic sites of 4 genes by real-time PCR. The levels of endothelin-1, sE-selectin, sP-selectin were determined by the ELISA technique.
Results. We determined that the T allele (G/T genotype) of rs5370 polymorphic site of EDN1 gene have a risk effect on IE in the superdominant mode of inheritance (OR=1,58, 95% CI=1,05-2,35, p=0,027). At the same time, the association between levels of endothelin-1, sE and sP selectins and carriage of the variable genotypes of the corresponding genes was not found. We noted that serum concentrations of biologically active endothelial proteins differ between patients with IE and healthy individuals.
Conclusion. The study confirms the presence of endothelial dysfunction markers in the blood of patients with IE. It shows the association between rs5370 site of EDN1 gene and an increased risk of IE in heterozygous carriers of the minor T allele. However, additional research is needed to confirm these observations and to get detailed description of how gene variability determines underlying risk for IE.
About the Authors
A. V. PonasenkoRussian Federation
Kemerovo.
A. V. Tsepokina
Russian Federation
Kemerovo.
A. G. Kutixin
Russian Federation
Kemerovo.
Yu. A. Kudryavtseva
Russian Federation
Kemerovo.
References
1. Habib G, Lancellotti P, Antunes M, et al. 2015 ESC guidelines for the management of infective endocarditis. Russian Journal of Cardiology. 2016;21(5):65-116. (In Russ.). doi:10.15829/1560-4071-2016-5-65-116.
2. Gurevich MA. Several points about infective endocarditis in present-day practice. Almanac of Clinical Medicine. 2014;(35):30-3. (In Russ.). doi:10.18786/2072-0505-2014-35-30-33.
3. Faraji R, Behjati-Ardakani M, Moshtaghioun SM, et al. The diagnosis of microorganism involved in infective endocarditis (IE) by polymerase chain reaction (PCR) and real-time PCR: A systematic review. The Kaohsiung journal of medical sciences. 2018;34(2):71-8. doi:10.1016/j.kjms.2017.09.011.
4. Jans C, Boleij A. The road to infection: Host-microbe interactions defining the pathogenicity of Streptococcus bovis/Streptococcus equinus complex members. Frontiers in microbiology. 2018;9:603. doi:10.3389/fmicb.2018.00603.
5. Mevada V, Patel R, Patel B, et al. Comparative homology model building and docking evaluation for RNA III inhibiting peptide of Multi drug resistant Staphylococcus aureus strain MRSA252. ComputBiol Chem. 2018;73:189-99. doi:10.1016/j.compbiolchem.2018.02.011.
6. Boujelben I, Gdoura R, Hammami A. A broad-range PCR technique for the diagnosis of infective endocarditis. Brazilian Journal of Microbiology. 2018. doi:10.1016/j.bjm.2017.03.019.
7. Domitrovic TN, Hujer AM, Perez F, et al. Multidrug Resistant Pseudomonas aeruginosa Causing Prosthetic Valve Endocarditis: A Genetic-Based Chronicle of Evolving Antibiotic Resistance. In Open forum infectious diseases. 2016;3(4):ofw188. doi: 10.1093/ofid/ofw188.
8. Hoen B, Duval X. Epidemiology of infective endocarditis. La Revue du praticien. 2012;62(4):511-4.
9. Golias C, Batistatou A, Bablekos G, et al. Physiology and pathophysiology of selectins, integrins, and IgSF cell adhesion molecules focusing on inflammation. A paradigm model on infectious endocarditis. Cell communication & adhesion. 2011;18(3):19-32. doi:10.3109/15419061.2011.606381.
10. Barthel SR, Gavino JD, Descheny L, et al. Targeting selectins and selectin ligands in inflammation and cancer. Expert opinion on therapeutic targets. 2007; 11(11): 1473-91. doi:10.1517/14728222.11.11.1473.
11. Ponasenko AV, Khutornaya MV, Antonova LV, et al. Dynamics of concentration of cell adhesion molecules at formation systemic inflammatory response after surgery acquired heart diseases. Fundamental research. 2014;7-3:549-53. (In Russ.).
12. Habib G, Hoen B, Tornos P, et al. ESC Committee for Practice Guidelines. Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and the International Society of Chemotherapy (ISC) for Infection and Cancer. Eur. Heart J. 2009;30,19:2369-413.
13. Inzhutova AI, Larionov AA, Salmina AB, et al. Molecular and cellular mechanisms of endothelial dysfunction in different pathology. report 1. Siberian Medical Journal (Irkutsk). 2010;5:85-8. (In Russ.).
14. Popova AA, Berezikova EN, Mayanskaya SD. Mechanism of endothelial dysfunction development. Siberian Medical Review. 2010;64(4):7-11. (In Russ.).
15. Dremina NN, Shurygin MG, Shurygina !А. Endothelin is normal and with pathology. International Journal of Applied and Fundamental Research. 2016;10(2):210-4. (In Russ.).
16. Hwang SJ, Ballantyne CM, Sharrett AR, et al. Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases: the Atherosclerosis Risk In Communities (ARIC) study. Circulation. 1997;96(12):4219-25. doi:10.1161/01.CIR.96.12.4219.
17. Yagoda AV, Koroj PV, Gilyazova GI. Selectins as predictors of stable virological clearance in chronic viral hepatitis C. Medical news of north Caucasus. 2013;8(3):5-9. (In Russ.). doi:10.14300/mnnc.2013.08001.
18. Janeway C. Immunobiology: the immune system in health and disease. New York: Garland Science. 2005. ISBN 0-8153-4101-6.
19. Wang J, Li J, Liu Q. Association between platelet activation and fibrinolysis in acute stroke patients. Neurosci. Lett. 2005;384(3):305-9. doi:101016/j.neulet.2005.04.090.
20. Ponasenko AV, Khutornaya MV, Golovkin AS, et al. Potential role as a proinflammatory cytokines in postoperative severe systemic inflammatory response syndrome undergoing heart valve replacement surgery. Complex Issues of Cardiovascular Diseases. 2013;(4):71-6. (In Russ.).
21. Moreau K, Clemenceau A, Le Moing V, et al. Human Genetic Susceptibility to Native Valve Staphylococcus aureus Endocarditis in Patients With S. aureus Bacteremia: Genome-Wide Association Study. Frontiers in microbiology 2018; 9: 640. doi:10.3389/fmicb.2018.00640.
22. Golovkin AS, Ponasenko AV, Yuzhalin AE, et al. An association between single nucleotide polymorphisms within TLR and TREM-1 genes and infective endocarditis. Cytokine. 2015;71:16-21. doi:10.1016/j.cyto.2014.08.001.
23. Ponasenko AV, Kutikhin AG, Khutornaya MV, et al. Inherited variation in cytokine, acute phase response, and calcium metabolism genes affects susceptibility to infective endocarditis. Mediators Inflamm. 2017;1-21. doi:10.1155/2017/7962546.
24. Weinstock M, Grimm I, Dreier J, et al. Genetic variants in genes of the inflammatory response in association with infective endocarditis. PLoS One. 2014;9(10):e110151. doi:10.1371/journal.pone.0110151.
25. Bustamante J, Tamayo E, Florez S, et al. Toll-like receptor 2 R753Q polymorphisms are associated with an increased risk of infective endocarditis Rev EspCardiol. 2011;64(11):1056-9. doi:10.1016/j.recesp.2011.02.024.
26. Kerrigan SW, McDonnell C. Dysregulation of the endothelium following Staphylococcus aureus infection. BiochemSoc Trans. 2015;43(4):715-9. doi:10.1042/BST20140309.
Review
For citations:
Ponasenko A.V., Tsepokina A.V., Kutixin A.G., Kudryavtseva Yu.A. Polymorphism of protein genes associated with endothelial function in patients with infective endocarditis. Russian Journal of Cardiology. 2018;(10):88-97. (In Russ.) https://doi.org/10.15829/1560-4071-2018-10-88-97