Clinical Physiology of Circulation

Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery


Issues of genetics and the risk of development of severe infectious complications and sepsis in cardiovascular surgery. Part 4

Authors: Koksheneva I.V., Zakaraya I.T., Maloroeva A.I., Iraskhanov A.Sh.

Company:
Bakoulev National Medical Research Center for Cardiovascular Surgery, Moscow, Russian Federation

E-mail: Сведения доступны для зарегистрированных пользователей.

DOI: https://doi.org/10.24022/1814-6910-2021-18-4-261-272

UDC: 616.94:616.12-089.168-06

Link: Clinical Physiology of Blood Circulaiton. 2021; 4 (18): 261-272

Quote as: Koksheneva I.V., Zakaraya I.T., Maloroeva A.I., Iraskhanov A.Sh. Issues of genetics and the risk of development of severe infectious complications and sepsis in cardiovascular surgery. Part 4. Clinical Physiology of Circulation. 2021; 18 (4): 261–72 (in Russ.). DOI: 10.24022/1814-6910-2021-18-4-261-272

Received / Accepted:  07.10.2021 / 29.10.2021

Full text:
Subscribe 🔒

Abstract

Despite advances in the prevention and treatment of infectious complications after cardiac surgery, sepsis remains a serious problem. Immune dysfunction is the main pathophysiological process that develops in septic patients. An imbalanced immune response is responsible for a significant percentage of negative outcomes in critically ill patients. The predisposition to a severe course of the infectious process has a genetic component. Accordingly, the genetic variability that disrupts the immune response to the introduction of infectious agents may explain the ability of the immune system to respond differently to infection, the diversity of the clinical picture of the course of the infectious process, responses to treatment, and genetic predisposition to infection in each individual patient. Identification of such genetic variants can identify patients at high risk of developing sepsis and organ dysfunction during infectious processes. This review presents published data on the identified genetic variants associated with inflammatory cascades and regulatory pathways associated with severe infection and sepsis. The results of published studies on the identification of key candidate genes involved in inflammatory signaling pathways may be useful for stratification of the risk of sepsis, monitoring its development, and prognosis, while their specific functions and mechanisms during the development of the infectious process and sepsis require further study. It is likely that in the future, genotyping will be included in the routine assessment of critically ill patients and will help develop the most effective treatment modalities.

References

  1. Гельфанд Б.Р. (ред.) Сепсис: классификация, клинико-диагностическая концепция и лечение. 4-е изд., доп. и перераб. М.: ООО «Медицинское информационное агентство»; 2017.
  2. Mayr F.B., Yende S., Angus D.C. Epidemiology of severe sepsis. Virul. Land. Biosci. 2014; 5 (1): 4–11. DOI: 10.4161/viru.27372
  3. Belopolskaya O.B., Smelaya T.V., Moroz V.V., Golubev A.M., Salnikova L.E. Clinical associations of host genetic variations in the genes of cytokines in critically ill patient. Clin. Exp. Immunol. 2015; 180 (3): 531–41. DOI: 10.1111/cei.12592
  4. Rittirsch D., Huber-Lang M.S., Flierl M.A., Ward P.A. Immunodesign of experimental sepsis by cecal ligation and puncture. Nat. Protoc. 2009; 4 (1): 31–6. DOI: 10.1038/nprot.2008.214
  5. Giamarellos-Bourboulis E.J., Opal S.M. The role of genetics and antibodies in sepsis. Ann. Transl. Med. 2016; 4 (17): 328–40. DOI: 10.21037/atm.2016.08.63
  6. Angus D.C., Wax R.S. Epidemiology of sepsis: an update. Crit. Care. Med. 2001; 29 (Suppl. 7): S109–16. DOI: 10.1097/00003246-200107001-00035
  7. Surbatovic M., Veljovic M., Jevdjic J., Popovic N., Djordjevic D., Radakovic S. Immunoinflammatory response in critically ill patients: severe sepsis and/or trauma. Mediat. Inflamm. 2013; 2013: 362793. DOI: 10.1155/2013/362793
  8. Mira J.P., Cariou A., Grall F., Delclaux C., Losser M.R., Heshmati F. et al. Association of TNF2, a TNF-alpha promoter polymorphism, with septic shock susceptibility and mortality: a multicenter study. JAMA. 1999; 282 (6): 561–8. DOI: 10.1001/jama.282.6.561
  9. McGuire W., Hill A.V., Allsopp C.E., Greenwood B.M., Kwiatkowski D. Variation in the TNF-alpha promoter region associated with susceptibility to cerebral malaria. Nature. 1994; 371 (6497): 508–10. DOI: 10.1038/371508a0
  10. Nadel S., Newport M.J., Booy R., Levin M. Variation in the tumor necrosis factor-alpha gene promoter region may be associated with death from meningococcal disease. J. Infect. Dis. 1996; 174 (4): 878–80. DOI: 10.1093/infdis/174.4.878
  11. Gordon A.C., Waheed U., Hansen T.K., Hitman G.A., Garrard C.S., Turner M.W. et al. Mannose-binding lectin polymorphisms in severe sepsis: relationship to levels, incidence, and outcome. Shock. 2006; 25 (1): 88–93. DOI: 10.1097/01.shk.0000186928.57109.8d
  12. Jabandziev P., Smerek M., Michalek J., Fedora M., Kosinova L., Hubacek J.A., Michalek J. Multiple geneto-gene interactions in children with sepsis: a combination of five gene variants predicts outcome of lifethreatening sepsis. Crit. Care. 2014; 18 (1): 1. DOI: 10.1186/cc13174
  13. Kothari N., Bogra J., Abbas H., Kohli M., Malik A., Kothari D. et al. Tumor necrosis factor gene polymorphism results in high TNF level in sepsis and septic shock. Cytokine. 2013; 61 (2): 676–81. DOI: 10.1016/j.cyto.2012.11.016
  14. Allam G., Alsulaimani A.A., Alzaharani A.K., Nasr A. Neonatal infections in Saudi Arabia: association with cytokine gene polymorphisms. Cent. Eur. J. Immunol. 2015; 40 (1): 68–77. DOI: 10.5114/ceji.2015.50836
  15. Kotsaki A., Raftogiannis M., Routsi C., Baziaka F., Kotanidou A., Antonopoulou A. et al. Genetic polymorphisms within tumor necrosis factor gene promoter region: a role for susceptibility to ventilator-associated pneumonia. Cytokine. 2012; 59 (2): 358–63. DOI: 10.1016/j.cyto.2012.04.040
  16. Gao J.W., Zhang A.Q., Pan W., Yue C.L., Zeng L., Gu W., Jiang J. Association between IL-6-174G/C polymorphism and the risk of sepsis and mortality: a systematic review and meta-analysis. PLoS. One. 2015; 10 (3): e0118843. DOI: 10.1371/journal.pone.0118843
  17. Miguel-Bayarri V., Casanoves-Laparra E.B., Pallás-Beneyto L., Sancho-Chinesta S., Martín-Osorio L.F., Tormo-Calandín C., Bautista-Rentero D. Prognostic value of the biomarkers procalcitonin, interleukin-6 and C-reactive protein in severe sepsis. Med. Intensiva. 2012; 36 (8): 556–62. DOI: 10.1016/j.medin.2012.01.014
  18. Palmiere C., Augsburger M. Markers for sepsis diagnosis in the forensic setting: state of the art. Croat. Med. J. 2014; 55 (2): 103–14. DOI: 10.3325/cmj.2014.55.103
  19. Faix J.D. Biomarkers of sepsis. Crit. Rev. Clin. Lab. Sci. 2013; 50 (1): 23–36. DOI: 10.3109/10408363.2013.764490
  20. Martín-Loeches I., Solé-Violán J., Rodríguez de Castro F., García-Laorden M.I., Borderías L., Blanquer J. et al. Variants at the promoter of the interleukin-6 gene are associated with severity and outcome of pneumococcal community-acquired pneumonia. Intensive. Care. Med. 2012; 38 (2): 256–62. DOI: 10.1007/s00134-011-2406-y
  21. Georgescu A.M., Grigorescu B.L., Chirtes, I.R., Vitin A.A., Fodor R.S,. The relevance of coding gene polymorphysms of cytokines and cellular receptors in sepsis. J. Crit. Care. Med. (Targu Mures). 2017; 3 (1): 5–11. DOI: 10.1515/jccm-2017-0001
  22. Surbatovic M., Grujic K., Cikota B., Jevtic M., Filipovic N., Romic P. et al. Polymorphisms of genes encoding tumor necrosis factor-alpha, interleukin-10, cluster of differentiation-14 and interleukin-1ra in critically ill patients. J. Crit. Care. 2010; 25 (3): 542.e1–8. DOI: 10.1016/j.jcrc.2009.12.003
  23. Ouyang L., Lv Y.D., Hou C., Wu G.B., He Z.H. Quantitative analysis of the association between interleukin-10 1082A/G polymorphism and susceptibility to sepsis. Mol. Biol. Rep. 2013; 40 (7): 4327–32. DOI: 10.1007/s11033-013-2520-8
  24. Pan W., Zhang A.Q., Yue C.L., Gao J.W., Zeng L., Gu W., Jiang J.X. Association between interleukin-10 polymorphisms and sepsis: a meta-analysis. Epidemiol. Infect. 2015; 143 (2): 366–75. DOI: 10.1017/S0950268814000703
  25. Stanilova S.A., Miteva L.D., Karakolev Z.T., Stefanov C.S. Interleukin-10-1082 promoter polymorphism in association with cytokine production and sepsis susceptibility. Intensive. Care. Med. 2006; 32 (2): 260–6. DOI: 10.1007/s00134-005-0022
  26. Zeng L., Gu W., Chen K., Jiang D., Zhang L., Du D. et al. Clinical relevance of the interleukin-10 promoter polymorphisms in Chinese Han patients with major trauma: genetic association studies. J. Crit. Care. 2009; 13 (6): R188. DOI: 10.1186/cc8182
  27. Accardo Palumbo A., Forte G.I., Pileri D., Vaccarino L., Conte F., D'Amelio L. et al. Analysis of IL-6, IL-10 and IL-17 genetic polymorphisms as risk factors for sepsis development in burned patients. Burns. 2012; 38 (2): 208–13. DOI: 10.1016/j.burns.2011.07.022
  28. Kofoed K., Andersen O., Kronborg G., Tvede M., Petersen J., Eugen-Olsen J., Larsen K. Use of plasma C-reactive protein, procalcitonin, neutrophils, macrophage migration inhibitory factor, soluble urokinase-type plasminogen activator receptor, and soluble triggering receptor expressed on myeloid cells-1 in combination to diagnose infections: a prospective study. Crit. Care. 2007; 11 (2): R38. DOI: 10.1186/cc5723
  29. Lorenz E., Mira J.P., Frees K.L., Schwartz D.A. Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock. Arch. Intern. Обзоры 271 Клиническая физиология кровообращения. 2021; 18 (4). DOI: 10.24022/1814-6910-2021-18-4-261-272 Med. 2002; 162 (9): 1028–32. DOI: 10.1001/archinte.162.9.1028
  30. Schlüter B., Raufhake C., Erren M., Schotte H., Kipp F., Rust S. et al. Effect of the interleukin-6 promoter polymorphism (-174 G/C) on the incidence and outcome of sepsis. Crit. Care. Med. 2002; 30 (1): 32–7. DOI: 10.1097/00003246-200201000-00005
  31. Oku R., Oda S., Nakada T.A., Sadahiro T., Nakamura M., Hirayama Y. et al. Differential pattern of cellsurface and soluble TREM-1 between sepsis and SIRS. Cytokine. 2013; 61 (1): 112–7. DOI: 10.1016/j.cyto.2012.09.003
  32. Peng L.S., Li J., Zhou G.S., Deng L.H., Yao H.G. Relationships between genetic polymorphisms of triggering receptor expressed on myeloid cells-1 and septic shock in a Chinese Han population. World J. Emerg. Med. 2015; 6 (2): 123–30. DOI: 10.5847/wjem.j.1920- 8642.2015.02.007
  33. Lemarié J., Barraud D., Gibot S. Host response biomarkers in sepsis: overview on sTREM-1 detection. Methods. Mol. Biol. 2015; 1237: 225–39. DOI: 10.1007/978-1-4939-1776-1_17
  34. West S.D., Ziegler A., Brooks T., Krencicki M., Myers O., Mold C. An FcγRIIa polymorphism with decreased C-reactive protein binding is associated with sepsis and decreased monocyte HLA-DR expression in trauma patients. J. Trauma. Acute. Care. Surg. 2015; 79 (5): 773–81. DOI: 10.1097/TA.0000000000000837
  35. Garnacho-Montero J., García-Cabrera E., JiménezÁlvarez R., Díaz-Martín A., Revuelto-Rey J., AznarMartín J., Garnacho-Montero C. Genetic variants of the MBL2 gene are associated with mortality in pneumococcal sepsis. Diagn. Microbiol. Infect. Dis. 2012; 73 (1): 39–44. DOI: 10.1016/j.diagmicrobio.2012.02.002
  36. Lu H., Wen D., Wang X., Gan L., Du J., Sun J. et al. Host genetic variants in sepsis risk: a field synopsis and meta-analysis. Crit. Care. 2019; 23 (1): 26. DOI: 10.1186/s13054-019-2313-0
  37. Man M., Close S.L., Shaw A.D., Bernard G.R., Douglas I.S., Kaner R.J. et al. Beyond single-marker analyses: mining whole genome scans for insights into treatment responses in severe sepsis. Pharmacogenomics. J. 2013; 13 (3): 218–26. DOI: 10.1038/tpj.2012.1
  38. Rautanen A., Chapman S.J., Hinds C.J. Response to Schöneweck et al. Common genomic variation in the FER gene: useful to stratify patients with sepsis due to pneumonia? Intensive. Care. Med. 2015; 41 (7): 1382. DOI: 10.1007/s00134-015-3893-z
  39. Scherag A., Schöneweck F., Kesselmeier M., Taudien S., Platzer M., Felder M. et al. Genetic factors of the disease course after sepsis: a genome-wide study for 28 day mortality. EBioMedicine. 2016; 12: 239–46. DOI: 10.1016/j.ebiom.2016.08.043
  40. Rosier F., Brisebarre A., Dupuis C., Baaklini S., Puthier D., Brun Ch. et al. Genetic predisposition to the mortality in septic shock patients: from GWAS to the identification of a regulatory variant modulating the activity of a CISH Enhancer. Int. J. Mol. Sci. 2021; 22 (11): 5852–80. DOI: 10.3390/ijms22115852
  41. Wang T., Wang Zh., Wang L., Yan Li, Wan J., Zhang Sh. et al. CRISPLD2 is expressed at low levels during septic shock and is associated with procalcitonin. PLoS. One. 2013; 8 (6): e65743. DOI: 10.1371/journal. pone.0065743
  42. Khor C.C., Vannberg F.O., Chapman S.J., Guo H., Wong S.H., Walley A.J. et al. CISH and susceptibility to infectious diseases. N. Engl. J. Med. 2010; 362 (22): 2092–101. DOI: 10.1056/NEJMoa0905606
  43. Zhang A., Gu W., Lu H., Zeng L., Zhang L., Du D. et al. Genetic contribution of suppressor of cytokine signalling polymorphisms to the susceptibility to infection after traumatic injury. Clin. Exp. Immunol. 2018; 194 (1): 93–102. DOI: 10.1111/cei.13160
  44. Lu X., Xue L., Sun W., Ye J., Zhu Zh, Mei H. Identification of key pathogenic genes of sepsis based on the gene expression omnibus database. Mol. Med. Rep. 2018; 17 (2): 3042–54. DOI: 10.3892/mmr.2017.8258
  45. Hall M.W., Gavrilin M.A., Knatz N.L., Duncan M.D., Fernandez S.A., Wewers M.D. Monocyte mRNA phenotype and adverse outcomes from pediatric multiple organ dysfunction syndrome. Pediatr. Res. 2007; 62 (5): 597–603. DOI: 10.1203/PDR.0b013e3181559774
  46. Hirata Y., Mitaka C., Sato K., Nagura T., Tsunoda Y., Amaha K., Marumo F. Increased circulating adrenomedullin, a novel vasodilatory peptide, in sepsis. J. Clin. Endocrinol. Metab. 1996; 81 (4): 1449–53. DOI: 10.1210/jcem.81.4.8636349
  47. Peters-Golden M., Henderson W.R. Leukotrienes. N. Engl. J. Med. 2007; 357 (18): 1841–54. DOI: 10.1056/NEJMra071371
  48. Monteiro A.P., Soledade E., Pinheiro C.S., DellatorreTeixeira L., Oliveira G.P., Oliveira M.G. et al. Pivotal role of the 5-lipoxygenase pathway in lung injury after experimental sepsis. Am. J. Respir. Cell. Mol. Biol. 2014; 50 (1): 87–95. DOI: 10.1165/rcmb.2012- 0525OC
  49. Jin L.Y., Li C.F., Zhu G.F., Wu C.T., Wang J., Yan S.F. Effect of siRNA against NF-kB on sepsis induced acute lung injury in a mouse model. Mol. Med. Rep. 2014; 10 (2): 631–7. DOI: 10.3892/mmr.2014.2299
  50. Zhang Li-Na, Wang X., Wu L., Huang L., Zhao C., Peng Q., Ai Y. Diagnostic and predictive levels of calcium-binding protein A8 and tumor necrosis factor receptor-associated factor 6 in sepsis-associated encephalopathy: a prospective observational study. Chin. Med. J. 2016; 129 (14): 1674–81. DOI: 10.4103/0366-6999.185860
  51. Buhimschi C.S., Bhandari V., Dulay A.T., Nayeri U.A., Abdel-Razeq S.S., Pettker C.M. et al. Proteomics mapping of cord blood identifies haptoglobin "switch-on" pattern as biomarker of early-onset neonatal sepsis in preterm newborns. PLoS. One. 2011; 6 (10): e26111. DOI: 10.1371/journal.pone.0026111
****
  1. Gelfand B.R. (Ed.) Sepsis: classification, clinical diagnostic concept and treatment. 4th edn, rev. and upd. Moscow; 2017 (in Russ.).
  2. Mayr F.B., Yende S., Angus D.C. Epidemiology of severe sepsis. Virul. Land. Biosci. 2014; 5 (1): 4–11. DOI: 10.4161/viru.27372
  3. Belopolskaya O.B., Smelaya T.V., Moroz V.V., Golubev A.M., Salnikova L.E. Clinical associations of host genetic variations in the genes of cytokines in critically ill patient. Clin. Exp. Immunol. 2015; 180 (3): 531–41. DOI: 10.1111/cei.12592
  4. Rittirsch D., Huber-Lang M.S., Flierl M.A., Ward P.A. Immunodesign of experimental sepsis by cecal ligation and puncture. Nat. Protoc. 2009; 4 (1): 31–6. DOI: 10.1038/nprot.2008.214
  5. Giamarellos-Bourboulis E.J., Opal S.M. The role of genetics and antibodies in sepsis. Ann. Transl. Med. 2016; 4 (17): 328–40. DOI: 10.21037/atm.2016.08.63
  6. Angus D.C., Wax R.S. Epidemiology of sepsis: an update. Crit. Care. Med. 2001; 29 (Suppl. 7): S109–16. DOI: 10.1097/00003246-200107001-00035
  7. Surbatovic M., Veljovic M., Jevdjic J., Popovic N., Djordjevic D., Radakovic S. Immunoinflammatory response in critically ill patients: severe sepsis and/or trauma. Mediat. Inflamm. 2013; 2013: 362793. DOI: 10.1155/2013/362793
  8. Mira J.P., Cariou A., Grall F., Delclaux C., Losser M.R., Heshmati F. et al. Association of TNF2, a TNF-alpha promoter polymorphism, with septic shock susceptibility and mortality: a multicenter study. JAMA. 1999; 282 (6): 561–8. DOI: 10.1001/jama.282.6.561
  9. McGuire W., Hill A.V., Allsopp C.E., Greenwood B.M., Kwiatkowski D. Variation in the TNF-alpha promoter region associated with susceptibility to cerebral malaria. Nature. 1994; 371 (6497): 508–10. DOI: 10.1038/371508a0
  10. Nadel S., Newport M.J., Booy R., Levin M. Variation in the tumor necrosis factor-alpha gene promoter region may be associated with death from meningococcal disease. J. Infect. Dis. 1996; 174 (4): 878–80. DOI: 10.1093/infdis/174.4.878
  11. Gordon A.C., Waheed U., Hansen T.K., Hitman G.A., Garrard C.S., Turner M.W. et al. Mannose-binding lectin polymorphisms in severe sepsis: relationship to levels, incidence, and outcome. Shock. 2006; 25 (1): 88–93. DOI: 10.1097/01.shk.0000186928.57109.8d
  12. Jabandziev P., Smerek M., Michalek J., Fedora M., Kosinova L., Hubacek J.A., Michalek J. Multiple geneto-gene interactions in children with sepsis: a combination of five gene variants predicts outcome of lifethreatening sepsis. Crit. Care. 2014; 18 (1): 1. DOI: 10.1186/cc13174
  13. Kothari N., Bogra J., Abbas H., Kohli M., Malik A., Kothari D. et al. Tumor necrosis factor gene polymorphism results in high TNF level in sepsis and septic shock. Cytokine. 2013; 61 (2): 676–81. DOI: 10.1016/j.cyto.2012.11.016
  14. Allam G., Alsulaimani A.A., Alzaharani A.K., Nasr A. Neonatal infections in Saudi Arabia: association with cytokine gene polymorphisms. Cent. Eur. J. Immunol. 2015; 40 (1): 68–77. DOI: 10.5114/ceji.2015.50836
  15. Kotsaki A., Raftogiannis M., Routsi C., Baziaka F., Kotanidou A., Antonopoulou A. et al. Genetic polymorphisms within tumor necrosis factor gene promoter region: a role for susceptibility to ventilator-associated pneumonia. Cytokine. 2012; 59 (2): 358–63. DOI: 10.1016/j.cyto.2012.04.040
  16. Gao J.W., Zhang A.Q., Pan W., Yue C.L., Zeng L., Gu W., Jiang J. Association between IL-6-174G/C polymorphism and the risk of sepsis and mortality: a systematic review and meta-analysis. PLoS. One. 2015; 10 (3): e0118843. DOI: 10.1371/journal.pone.0118843
  17. Miguel-Bayarri V., Casanoves-Laparra E.B., Pallás-Beneyto L., Sancho-Chinesta S., Martín-Osorio L.F., Tormo-Calandín C., Bautista-Rentero D. Prognostic value of the biomarkers procalcitonin, interleukin-6 and C-reactive protein in severe sepsis. Med. Intensiva. 2012; 36 (8): 556–62. DOI: 10.1016/j.medin.2012.01.014
  18. Palmiere C., Augsburger M. Markers for sepsis diagnosis in the forensic setting: state of the art. Croat. Med. J. 2014; 55 (2): 103–14. DOI: 10.3325/cmj.2014.55.103
  19. Faix J.D. Biomarkers of sepsis. Crit. Rev. Clin. Lab. Sci. 2013; 50 (1): 23–36. DOI: 10.3109/10408363.2013.764490
  20. Martín-Loeches I., Solé-Violán J., Rodríguez de Castro F., García-Laorden M.I., Borderías L., Blanquer J. et al. Variants at the promoter of the interleukin-6 gene are associated with severity and outcome of pneumococcal community-acquired pneumonia. Intensive. Care. Med. 2012; 38 (2): 256–62. DOI: 10.1007/s00134-011-2406-y
  21. Georgescu A.M., Grigorescu B.L., Chirtes, I.R., Vitin A.A., Fodor R.S,. The relevance of coding gene polymorphysms of cytokines and cellular receptors in sepsis. J. Crit. Care. Med. (Targu Mures). 2017; 3 (1): 5–11. DOI: 10.1515/jccm-2017-0001
  22. Surbatovic M., Grujic K., Cikota B., Jevtic M., Filipovic N., Romic P. et al. Polymorphisms of genes encoding tumor necrosis factor-alpha, interleukin-10, cluster of differentiation-14 and interleukin-1ra in critically ill patients. J. Crit. Care. 2010; 25 (3): 542.e1–8. DOI: 10.1016/j.jcrc.2009.12.003
  23. Ouyang L., Lv Y.D., Hou C., Wu G.B., He Z.H. Quantitative analysis of the association between interleukin-10 1082A/G polymorphism and susceptibility to sepsis. Mol. Biol. Rep. 2013; 40 (7): 4327–32. DOI: 10.1007/s11033-013-2520-8
  24. Pan W., Zhang A.Q., Yue C.L., Gao J.W., Zeng L., Gu W., Jiang J.X. Association between interleukin-10 polymorphisms and sepsis: a meta-analysis. Epidemiol. Infect. 2015; 143 (2): 366–75. DOI: 10.1017/S0950268814000703
  25. Stanilova S.A., Miteva L.D., Karakolev Z.T., Stefanov C.S. Interleukin-10-1082 promoter polymorphism in association with cytokine production and sepsis susceptibility. Intensive. Care. Med. 2006; 32 (2): 260–6. DOI: 10.1007/s00134-005-0022
  26. Zeng L., Gu W., Chen K., Jiang D., Zhang L., Du D. et al. Clinical relevance of the interleukin-10 promoter polymorphisms in Chinese Han patients with major trauma: genetic association studies. J. Crit. Care. 2009; 13 (6): R188. DOI: 10.1186/cc8182
  27. Accardo Palumbo A., Forte G.I., Pileri D., Vaccarino L., Conte F., D'Amelio L. et al. Analysis of IL-6, IL-10 and IL-17 genetic polymorphisms as risk factors for sepsis development in burned patients. Burns. 2012; 38 (2): 208–13. DOI: 10.1016/j.burns.2011.07.022
  28. Kofoed K., Andersen O., Kronborg G., Tvede M., Petersen J., Eugen-Olsen J., Larsen K. Use of plasma C-reactive protein, procalcitonin, neutrophils, macrophage migration inhibitory factor, soluble urokinase-type plasminogen activator receptor, and soluble triggering receptor expressed on myeloid cells-1 in combination to diagnose infections: a prospective study. Crit. Care. 2007; 11 (2): R38. DOI: 10.1186/cc5723
  29. Lorenz E., Mira J.P., Frees K.L., Schwartz D.A. Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock. Arch. Intern. Обзоры 271 Клиническая физиология кровообращения. 2021; 18 (4). DOI: 10.24022/1814-6910-2021-18-4-261-272 Med. 2002; 162 (9): 1028–32. DOI: 10.1001/archinte.162.9.1028
  30. Schlüter B., Raufhake C., Erren M., Schotte H., Kipp F., Rust S. et al. Effect of the interleukin-6 promoter polymorphism (-174 G/C) on the incidence and outcome of sepsis. Crit. Care. Med. 2002; 30 (1): 32–7. DOI: 10.1097/00003246-200201000-00005
  31. Oku R., Oda S., Nakada T.A., Sadahiro T., Nakamura M., Hirayama Y. et al. Differential pattern of cellsurface and soluble TREM-1 between sepsis and SIRS. Cytokine. 2013; 61 (1): 112–7. DOI: 10.1016/j.cyto.2012.09.003
  32. Peng L.S., Li J., Zhou G.S., Deng L.H., Yao H.G. Relationships between genetic polymorphisms of triggering receptor expressed on myeloid cells-1 and septic shock in a Chinese Han population. World J. Emerg. Med. 2015; 6 (2): 123–30. DOI: 10.5847/wjem.j.1920- 8642.2015.02.007
  33. Lemarié J., Barraud D., Gibot S. Host response biomarkers in sepsis: overview on sTREM-1 detection. Methods. Mol. Biol. 2015; 1237: 225–39. DOI: 10.1007/978-1-4939-1776-1_17
  34. West S.D., Ziegler A., Brooks T., Krencicki M., Myers O., Mold C. An FcγRIIa polymorphism with decreased C-reactive protein binding is associated with sepsis and decreased monocyte HLA-DR expression in trauma patients. J. Trauma. Acute. Care. Surg. 2015; 79 (5): 773–81. DOI: 10.1097/TA.0000000000000837
  35. Garnacho-Montero J., García-Cabrera E., JiménezÁlvarez R., Díaz-Martín A., Revuelto-Rey J., AznarMartín J., Garnacho-Montero C. Genetic variants of the MBL2 gene are associated with mortality in pneumococcal sepsis. Diagn. Microbiol. Infect. Dis. 2012; 73 (1): 39–44. DOI: 10.1016/j.diagmicrobio.2012.02.002
  36. Lu H., Wen D., Wang X., Gan L., Du J., Sun J. et al. Host genetic variants in sepsis risk: a field synopsis and meta-analysis. Crit. Care. 2019; 23 (1): 26. DOI: 10.1186/s13054-019-2313-0
  37. Man M., Close S.L., Shaw A.D., Bernard G.R., Douglas I.S., Kaner R.J. et al. Beyond single-marker analyses: mining whole genome scans for insights into treatment responses in severe sepsis. Pharmacogenomics. J. 2013; 13 (3): 218–26. DOI: 10.1038/tpj.2012.1
  38. Rautanen A., Chapman S.J., Hinds C.J. Response to Schöneweck et al. Common genomic variation in the FER gene: useful to stratify patients with sepsis due to pneumonia? Intensive. Care. Med. 2015; 41 (7): 1382. DOI: 10.1007/s00134-015-3893-z
  39. Scherag A., Schöneweck F., Kesselmeier M., Taudien S., Platzer M., Felder M. et al. Genetic factors of the disease course after sepsis: a genome-wide study for 28 day mortality. EBioMedicine. 2016; 12: 239–46. DOI: 10.1016/j.ebiom.2016.08.043
  40. Rosier F., Brisebarre A., Dupuis C., Baaklini S., Puthier D., Brun Ch. et al. Genetic predisposition to the mortality in septic shock patients: from GWAS to the identification of a regulatory variant modulating the activity of a CISH Enhancer. Int. J. Mol. Sci. 2021; 22 (11): 5852–80. DOI: 10.3390/ijms22115852
  41. Wang T., Wang Zh., Wang L., Yan Li, Wan J., Zhang Sh. et al. CRISPLD2 is expressed at low levels during septic shock and is associated with procalcitonin. PLoS. One. 2013; 8 (6): e65743. DOI: 10.1371/journal. pone.0065743
  42. Khor C.C., Vannberg F.O., Chapman S.J., Guo H., Wong S.H., Walley A.J. et al. CISH and susceptibility to infectious diseases. N. Engl. J. Med. 2010; 362 (22): 2092–101. DOI: 10.1056/NEJMoa0905606
  43. Zhang A., Gu W., Lu H., Zeng L., Zhang L., Du D. et al. Genetic contribution of suppressor of cytokine signalling polymorphisms to the susceptibility to infection after traumatic injury. Clin. Exp. Immunol. 2018; 194 (1): 93–102. DOI: 10.1111/cei.13160
  44. Lu X., Xue L., Sun W., Ye J., Zhu Zh, Mei H. Identification of key pathogenic genes of sepsis based on the gene expression omnibus database. Mol. Med. Rep. 2018; 17 (2): 3042–54. DOI: 10.3892/mmr.2017.8258
  45. Hall M.W., Gavrilin M.A., Knatz N.L., Duncan M.D., Fernandez S.A., Wewers M.D. Monocyte mRNA phenotype and adverse outcomes from pediatric multiple organ dysfunction syndrome. Pediatr. Res. 2007; 62 (5): 597–603. DOI: 10.1203/PDR.0b013e3181559774
  46. Hirata Y., Mitaka C., Sato K., Nagura T., Tsunoda Y., Amaha K., Marumo F. Increased circulating adrenomedullin, a novel vasodilatory peptide, in sepsis. J. Clin. Endocrinol. Metab. 1996; 81 (4): 1449–53. DOI: 10.1210/jcem.81.4.8636349
  47. Peters-Golden M., Henderson W.R. Leukotrienes. N. Engl. J. Med. 2007; 357 (18): 1841–54. DOI: 10.1056/NEJMra071371
  48. Monteiro A.P., Soledade E., Pinheiro C.S., DellatorreTeixeira L., Oliveira G.P., Oliveira M.G. et al. Pivotal role of the 5-lipoxygenase pathway in lung injury after experimental sepsis. Am. J. Respir. Cell. Mol. Biol. 2014; 50 (1): 87–95. DOI: 10.1165/rcmb.2012- 0525OC
  49. Jin L.Y., Li C.F., Zhu G.F., Wu C.T., Wang J., Yan S.F. Effect of siRNA against NF-kB on sepsis induced acute lung injury in a mouse model. Mol. Med. Rep. 2014; 10 (2): 631–7. DOI: 10.3892/mmr.2014.2299
  50. Zhang Li-Na, Wang X., Wu L., Huang L., Zhao C., Peng Q., Ai Y. Diagnostic and predictive levels of calcium-binding protein A8 and tumor necrosis factor receptor-associated factor 6 in sepsis-associated encephalopathy: a prospective observational study. Chin. Med. J. 2016; 129 (14): 1674–81. DOI: 10.4103/0366-6999.185860
  51. Buhimschi C.S., Bhandari V., Dulay A.T., Nayeri U.A., Abdel-Razeq S.S., Pettker C.M. et al. Proteomics mapping of cord blood identifies haptoglobin "switch-on" pattern as biomarker of early-onset neonatal sepsis in preterm newborns. PLoS. One. 2011; 6 (10): e26111. DOI: 10.1371/journal.pone.0026111

About Authors

  • Inna V. Koksheneva, Dr. Med. Sci., Senior Researcher; ORCID
  • Irakliy T. Zakaraya, Junior Researcher
  • Amina I. Maloroeva, Postgraduate
  • Atabi Sh. Iraskhanov, Resident Physician; ORCID

 If you found mistakes, select text and press Alt+A