The role of polymorphism and expression features of innate immune response receptors genes in the pathogenesis of infectious endocarditis
https://doi.org/10.15829/1560-4071-2018-10-145-150
Abstract
Infectious endocarditis (IE) is a disease, usually of bacterial nature, the mortality rate from which is in fourth place among other lethal infectious diseases. In recent years there has been a tendency to an increase of prosthetic valve IE cases. The problem of antibiotic resistance leading to a decrease in the effectiveness of therapy is relevant for IE. Development task of new effective methods of preventing this disease, as well as assessing the severity of its consequences, is extremely relevant, especially because of progression of personalized medicine. The immune response plays an important role in the pathogenesis of IE, while receptors of the innate immune response are of great importance in the development and progression of this disease. Polymorphism of genes encoding these receptors leads to a change in their functional activity, which determines the effectiveness of the organism response to infection. This review analyzes the effect of polymorphism of several innate immune response receptors genes, as well as changes in their expression in patients with IE, and shows their importance in development of the individual sensitivity of patients to this pathology.
Keywords
infectious endocarditis,
gene polymorphism,
mRNA,
gene expression,
innate immunity,
innate immune response receptors
Supporting agencies: The Siberian Branch of the Russian Academy of Sciences
About the Authors
M. Yu. Siniczkij
Research Institute for Complex Issues of Cardiovascular Diseases; Federal Research Center of Coal and Coal Chemistry
Russian Federation
Kemerovo.
Competing Interests: Конфликт интересов не заявлен.
Russian Federation
Kemerovo.
Competing Interests: Конфликт интересов не заявлен.
A. V. Ponasenko
Research Institute for Complex Issues of Cardiovascular Diseases
Russian Federation
Kemerovo.
Competing Interests: Конфликт интересов не заявлен.
Russian Federation
Kemerovo.
Competing Interests: Конфликт интересов не заявлен.
References
1. 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.
2. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications: A scientific statement for healthcare professionals from the American Heart Association. Circulation. 2015;132:1435-86.
3. Bai AD, Agarwal A, Steinberg M, et al. Clinical predictors and clinical prediction rules to estimate initial patient risk for infective endocarditis in Staphylococcus aureus bacteraemia: a systematic review and meta-analysis. Clin Microbiol Infect. 2017;23:900-6.
4. Stasev AN, Rutkovskaya NV, Kokorin SG, et al. Salmonella endocarditis of mitral valve: clinical observation. Complex Issues of Cardiovascular Diseases. 2017;6:123-6. (In Russ.).
5. Ponasenko AV, Kutikhin AG, Khutornaya MV, et al. Association of TREM-1 gene polymorphism with infective endocarditis. Russian Journal of Infection and Immunity. 2015;5:331-8. (In Russ.).
6. Kiefer T, Park L, Tribouilloy C, et al. Association between valvular surgery and mortality among patients with infective endocarditis complicated by heart failure. JAMA. 2011;306:2239-47.
7. Fowler VG, Boucher HW, Corey GR, et al. Daptomycin versus standard therapy for bacteremia and endocarditis caused by Staphylococcus aureus. N Engl J Med. 2006;355:653-65.
8. Bannay A, Hoen B, Duval X, et al. The impact of valve surgery on short- and long-term mortality in left-sided infective endocarditis: do differences in methodological approaches explain previous conflicting results? Eur Heart J. 2011;32:2003-15.
9. Sy RW, Bannon PG, Bayfield MS, et al. Survivor treatment selection bias and outcomes research: a case study of surgery in infective endocarditis. Circ Cardiovasc Qual Outcomes. 2009;2:469-74.
10. Habib G, Hoen B, Tornos P, et al. 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;30:2369-413.
11. Gould FK, Denning DW, Elliott TS, et al. Guidelines for the diagnosis and antibiotic treatment of endocarditis in adults: a report of the Working Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother. 2012;67:269-89.
12. 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:e110151.
13. Jung CJ, Zheng QH, Shieh YH, et al. Streptococcus mutans autolysin AtlA is a fibronectin- binding protein and contributes to bacterial survival in the bloodstream and virulence for infective endocarditis. Mol Microbiol. 2009;74:888-902.
14. Tyurin VP. Infectious endocarditis: guidelines. GEOTAR-Media Publ. Moscow: 2012 p. 368. (In Russ.).
15. Akira S. Innate immunity and adjuvants. Philos Trans R Soc Lond B Biol Sci. 2011;366:2748-55.
16. Ip WK, Takahashi K, Moore KJ, et al. Mannose-binding lectin enhances Toll-like receptors 2 and 6 signaling from the phagosome. J Exp Med. 2008;205:169-81.
17. Schroder K, Tschopp J. The inflammasomes. Cell. 2010;140:821-32.
18. Kovalchuk LV, Svitich OA, Gankovskaya LV, et al. The role of Toll-like receptors in pathogenesis of human infection. Kursk scientific and practical bulletin “Man and his health”. 2012; 2: 147-53. (In Russ.).
19. Vallejo JG. Role of toll-like receptors in cardiovascular diseases. Clin Sci. 2011;121:1-10.
20. Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell. 2010;140:805-20.
21. Bustamante J, Tamayo E, Florez S, et al. Toll-like receptor-2 R753Q polymorphisms are associated with an increased risk of infective endocarditis. Rev Esp Cardiol. 2011;64:1056-9.
22. Zeljic K, Supic G, Jovic N, et al. Association of TLR2, TLR3, TLR4 and CD14 genes polymorphisms with oral cancer risk and survival. Oral Dis. 2014;20:416-24.
23. Nachtigall I, Tamarkin A, Tafelski S, et al. Polymorphisms of the toll-like receptor 2 and 4 genes are associated with faster progression and a more severe course of sepsis in critically ill patients. J Int Med Res. 2014;42:93-110.
24. Ospelt C, Gay S. TLRs and chronic inflammation. Int J Biochem Cell Biol. 2010;42:495-505.
25. Ponasenko AV, Kutikhin AG, Khutornaya MV, et al. Polymorphisms within the genes encoding Toll-like receptors and risk of infective endocarditis. Medicina v Kuzbasse. 2015;14:4-10. (In Russ.).
26. Wurfel MM, Gordon AC, Holden TD, et al. Toll-like receptor 1 polymorphisms affect innate immune responses and outcomes in sepsis. Am J Respir Crit Care Med. 2008;178:710-20.
27. de Toledo A, Nagata E, Yoshida Y, et al. Streptococcus oralis coaggregation receptor polysaccharides induce inflammatory responses in human aortic endothelial cells. Mol Oral Microbiol. 2012;27:295-307.
28. Nagata E, Oho T. Invasive Streptococcus mutans induces inflammatory cytokine production in human aortic endothelial cells via regulation of intracellular TLR2 and NOD2. Mol Oral Microbiol. 2017;32:131-41.
29. Sabroe I, Parker LC, Dower SK, et al. The role of TLR activation in inflammation. J Pathol. 2008;214:126-35.
30. Echchannaoui H, Frei K, Schnell C, et al. Toll-like receptor 2-deficient mice are highly susceptible to Streptococcus pneumoniae meningitis because of reduced bacterial clearing and enhanced inflammation. J Infect Dis. 2002;186:798-806.
31. Cox D, Kerrigan SW, Watson SP. Platelets and the innate immune system: mechanisms of bacterial-induced platelet activation. J Thromb Haemost. 2011;9:1097-107.
32. Kawai T, Akira S. The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors. Nat Immunol. 2010;11:373-84.
33. Kawai T, Akira S. The roles of TLRs, RLRs and NLRs in pathogen recognition. Int Immunol. 2009;21:317-37.
34. Robertson J, Lang S, Lambert PA, et al. Peptidoglycan derived from Staphylococcus epidermidis induces Connexin-43 hemichannel activity with consequences on the innate immune response in endothelial cells. Biochem J. 2010;432:133-43.
35. Gottschalk M, Segura M, Xu J. Streptococcus suis infections in humans: the Chinese experience and the situation in North America. Anim Health Res Rev. 2007;8:29-45.
36. Zhang T, Kurita-Ochiai T, Hashizume T, et al. Aggregatibacter actinomycetemcomitans accelerates atherosclerosis with an increase in atherogenic factors in spontaneously hyperlipidemic mice. FEMS Immunol Med Microbiol. 2010;59:143-51.
37. Miettinen M, Veckman V, Latvala S, et al. Live Lactobacillus rhamnosus and Streptococcus pyogenes differentially regulate Toll-like receptor (TLR) gene expression in human primary macrophages. J Leukoc Biol. 2008;84:1092-100.
38. Hruz P, Zinkernagel AS, Jenikova G, et al. NOD2 contributes to cutaneous defense against Staphylococcus aureus through alpha-toxin-dependent innate immune activation. Proc Natl Acad Sci USA. 2009;106:12873-8.
Review
For citations:
Siniczkij M.Yu., Ponasenko A.V. The role of polymorphism and expression features of innate immune response receptors genes in the pathogenesis of infectious endocarditis. Russian Journal of Cardiology. 2018;(10):145-150. (In Russ.) https://doi.org/10.15829/1560-4071-2018-10-145-150
Views:
1087
Email this article 