Covid-19 Enfeksiyonunun ARDS komplikasyonunda IL-10 ve IL-10 (-1082G/A) Gen Varyasyonunun Potansiyel Rollerinin İncelenmesi

Yıl 2021, Cilt: 47 Sayı: 2, 313 - 321, 01.08.2021

Nevra Alkanlı Arzu Ay

https://doi.org/10.32708/uutfd.934904

Öz

COVID-19 yeni koronavirüs hastalığı olarak bilinmektedir ve COVID-19 enfeksiyonundan kaynaklanan komplikasyonlar yaş, cinsiyet ve komorbiditeler gibi çeşitli faktörlere bağlı olarak değişmektedir. Tüm yaş gruplarını etkileyebilen COVID-19 enfeksiyonu etkilenen popülasyonların bireysel özelliklerine bağlı olarak doğrulanmış vakaların bir kısmında ciddi rahatsızlık ve ölüm nedeni olarak ortaya çıkabilmektedir. Bu enfeksiyon özellikle yaşlı bireylerde ve hipertansiyon, diabetes mellitus, astım gibi komorbiditelere sahip kişilerde daha şiddetli seyretmektedir. Ancak COVID-19 enfeksiyonunun oldukça genç olan bireylerde de görülebileceği bildirilmiştir. Bu yüzden doku proteinlerinin ekspresyon düzeyleri gibi intrinsik faktörlerin yanısıra, genetik varyasyonlar gibi genetik faktörler de enfeksiyon patogenezine katkıda bulunabilmektedir. COVID-19 hastalarının yarısından fazlasında en sık görülen komplikasyonlardan biri yoğun bakım tedavisi gerektiren ARDS (Akut Solunum Sıkıntısı Sendromu) dir. COVID-19’da viral enfeksiyona yanıt olarak İnterlökin-10 (IL-10) gibi sitokinler salınmaktadır. COVID-19 enfeksiyonu sırasında gelişen sitokin fırtınası kontrolsüz inflamasyona neden olmaktadır. Böylece çoklu organ yetmezlikle-ri gelişebilmekte ve ARDS ile ilişkili sendromlar indüklenebilmektedir. Sitokin fırtınası COVID-19 hastalarında anlamlı derecede artmış IL-10 düzeyleri ile ilişkilendirilmiştir. ARDS patogenezinde inflamasyon önemli bir belirteçtir. Proinflamatuar ve antiinflamatuar sitokinler arasındaki dengesizlik sonucunda ARDS gelişebilmektedir. IL-10 geninin promotör bölgelerindeki genetik varyasyonlar sonucunda IL-10 mRNA ve protein düzeylerinde değişiklikler ortaya çıkmaktadır. IL-10’un patolojik proinflamatuar işlevi engelleyerek COVID-19 enfeksiyonundaki mortalitenin azalmasına katkı sağlayabileceği düşünülmektedir. ARDS gelişen COVID-19 hastalarında IL-10 geninin promotör bölgesinde tanımlanan IL-10 (-1082G/A) gen varyasyonu genotip dağılımlarına göre IL-10 ekspresyon düzeylerinin belirlenmesi, ARDS’nin patolojik mekanizmalarının daha iyi anlaşılabilmesi ve ARDS’ye yönelik terapötik stratejilerin geliştirilebilmesi bakımından oldukça önemlidir. Bu derlemede COVID-19 enfeksiyonunda gelişen ARDS komplikasyonunda IL-10 ve IL-10 (-1082G/A) gen varyasyonlarının rolünün incelenmesi amaçlanmıştır.

Anahtar Kelimeler

COVID-19, Akut Solunum Sıkıntısı Sendromu, İnterlökin, Genetik Varyasyon

Destekleyen Kurum

Bu çalışma herhangi bir finansal kuruluş tarafından desteklenmemiştir.

Proje Numarası

Proje Numarası bulunmamaktadır.

Examination of the Potential Roles of IL-10 and IL-10 (-1082G/A) Gene Variation in ARDS Complication of COVID-19 Infection ARDS Complication of COVID-19 and IL-10 Gene Variation

Öz

COVID-19 is known as the novel coronavirus disease and complications proceed from COVID-19 infection vary depending on various factors such as age, gender and comorbidities. COVID-19 infection which can affect all age groups may occur as a cause of serious illness and death in some of the confirmed cases, depending on the individual characteristics of the affected populations. Therefore, besides intrinsic factors such as the expression levels of tissue proteins, genetic factors such as genetic variations may also contribute to the pathogenesis of the infection. One of the most common complications in COVID-19 patients is ARDS (Acute Respiratory Distress Syndrome). In COVID-19, cytokines such as IL-10 are released in response to viral infection. Cytokine storm that develops during COVID-19 infection causes uncontrolled inflammation. Thus, multiple organ failure can develop and ARDS-related syndromes can be induced. Cytokine storm has been associated with significantly increased IL-10 levels in COVID-19 patients. Changes occur in IL-10 mRNA and protein levels as a result of genetic variations in the promoter regions of the IL-10 gene. It is thought that IL-10 can contribute to the reduction of mortality in COVID-19 infection by preventing pathological proinflammatory function. Determining IL-10 expression levels according to IL-10 (-1082G/A) gene variation genotype distributions defined in the promoter region of IL-10 gene in COVID-19 patients with ARDS very important in terms of better understanding of the pathological mechanisms and developing of therapeutic strategies. In this review, it is aimed to examine the role of IL-10 and IL-10 (-1082G/A) gene variation in ARDS complication of COVID-19 infection.

Anahtar Kelimeler

COVID-19, Acute Respiratory Distress Syndrome, Interleukin, Genetic Variation

Proje Numarası

Proje Numarası bulunmamaktadır.

Kaynakça

• 1. Öztürk R, Taşova Y, Ayaz A. COVID-19: pathogenesis, genetic polymorphism, clinical features and laboratory findings. Turk J Med Sci. 2020;50:638-657. doi:10.3906/sag-2005-287.
• 2. Sungnak W, Huang N, Bécavin C et al. SARSCoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes. Nature Medicine. 2020;26(5): 681-687. doi: 10.1038/s41591-020-0868-6.
• 3. Ulrich H, Pillat MM. CD147 as a target for COVID-19 treatment: suggested effects of azithromycin and stem cell engagement. Stem Cell Reviews and Reports. 2020;16:434-440. doi: 10.1007/s12015-020-09976-7.
• 4. Montenegro F, Unigarro L, Paredes G et al. Acute respiratory distress syndrome (ARDS) caused by the novel coronavirus disease (COVID-19): a practical comprehensive literature review. Expert Rev Respir Med. 2021;15(2):183-195. doi: 10.1080/17476348.2020.1820329.
• 5. Mulinari Turin de Oliveira N, Fernandes da Silva Figueiredo I, Cristine Malaquias da Silva L et al. Tissue Proteases and Immune Responses: Influencing Factors of COVID-19 Severity and Mortality. Pathogens. 2020;9(10):817. doi: 10.3390/pathogens9100817.
• 6. Jin Y, Yang H, Ji W et al. Virology, epidemiology, pathogenesis, and control of COVID-19. Viruses. 2020;12 (4):372. doi: 10.3390/v12040372.
• 7. Zou X, Chen K, Zou J et al. The single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable toWuhan 2019-nCoV infection. Frontiers in Medicine. 2020;14(2):185-192. doi: 10.1007/s11684-020-0754-0.
• 8. Xiao F, Tang M, Zheng X et al. Evidence for gastrointestinal infection of SARS-CoV-2. Gastroenterology. 2020;158(6):1831-1833.e3. doi: 10.1053/j.gastro.2020.02.055.
• 9. Zhou Y, Zhang Z, Tian J et al. Risk factors associated with disease progression in a cohort of patients infected with the 2019 novel coronavirus. Annals of Palliative Medicine. 2020;9(2):428-436. doi: 10.21037/apm.2020.03.26.
• 10. Grasselli G, Zangrillo A, Zanella A et al. Baseline characteristics and outcomes of 1591 patients infected with SARS-CoV-2 admitted to ICUs of the Lombardy Region, Italy. The Journal of the American Medical Association. 2020;323(16):1574-1581. doi: 10.1001/jama.2020.53948.
• 11. Cheng Y, Luo R, Wang K et al. Kidney disease is associated with in-hospital death of patients with COVID-19. Kidney International. 2020;97(5):829-838. doi: 10.1016/j.kint.2020.03.005.
• 12. Coutard B, Valle C, de Lamballerie X et al. The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade. Antiviral Res. 2020;176:104742. doi: 10.1016/j.antiviral.2020.104742.
• 13. Hoffmann M, Kleine-Weber H, Schroeder S et al. SARS-CoV-2 Cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020;181(2):271-280.e8. doi: 10.1016/j.cell.2020.02.052.
• 14. Xu Z, Shi L, Wang Y et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020;8(4):420-422. doi: 10.1016/S2213-2600(20)30076-X.
• 15. Wu F, Zhao S, Yu B et al. A new coronavirus associated with human respiratory disease in China. Nature. 2020;579:265-269. doi: 10.1038/s41586-020-2008-3.
• 16. Qin C, Zhou L, Hu Z et al. Dysregulation of Immune Response in Patients With Coronavirus 2019 (COVID-19) in Wuhan, China. Clin Infect Dis. 2020;28:71(15):762-768. doi: 10.1093/cid/ciaa248.
• 17. Thevarajan I, Nguyen THO, Koutsakos M et al. Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19. Nat Med. 2020;26(4):453-455. doi: 10.1038/s41591-020-0819-2.
• 18. Zuo Y, Yalavarthi S, Shi H et al. Neutrophil extracellular traps in COVID-19. JCI Insight. 2020;4:5(11):e138999. doi: 10.1172/jci.insight.138999.
• 19. McFadyen JD, Stevens H, Peter K. The Emerging Threat of (Micro) Thrombosis in COVID-19 and Its Therapeutic Implications. Circ Res. 2020;31:127(4):571-587. doi: 10.1161/CIRCRESAHA.120.317447.
• 20. Guo YR, Cao QD, Hong ZS et al. The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak - an update on the status. Mil Med Res. 2020;13:7(1):11. doi: 10.1186/s40779-020-00240-0.
• 21. Inciardi RM, Lupi L, Zaccone G et al. Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020;5(7):819-824. doi: 10.1001/jamacardio.2020.1096.
• 22. Shi S, Qin M, Shen B et al. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol. 2020;5(7):802-810. doi: 10.1001/jamacardio.2020.0950.
• 23. Wang D, Hu B, Hu C et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA. 2020;323(11):1061-1069. doi: 10.1001/jama.2020.1585.
• 24. Yang X, Yu Y, Xu J et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med. 2020;8(5):475-481. doi: 10.1016/S2213-2600(20)30079-5.
• 25. Jin X, Lian JS, Hu JH et al. Epidemiological, clinical and virological characteristics of 74 cases of coronavirus-infected disease 2019 (COVID-19) with gastrointestinal symptoms. Gut. 2020;69(6):1002-1009. doi: 10.1136/gutjnl-2020-320926.
• 26. Lin L, Jiang X, Zhang Z et al. Gastrointestinal symptoms of 95 cases with SARS-CoV-2 infection. Gut. 2020;69:997-1001. doi:10.1136/gutjnl-2020-321013.
• 27. Tian Y, Rong L, Nian W et al. Review article: gastrointestinal features in COVID-19 and the possibility of faecal transmission. Aliment Pharmacol Ther. 2020;51(9):843-851. doi: 10.1111/apt.15731.
• 28. Bello RO, Chin VK, Abd Rachman Isnadi MF et al. The Role, Involvement and Function(s) of Interleukin-35 and Interleukin-37 in Disease Pathogenesis. Int J Mol Sci. 2018;19(4):1149. doi: 10.3390/ijms19041149.
• 29. Gastl GA, Abrams JS, Nanus DM et al. Interleukin-10 production by human carcinoma cell lines and its relationship to interleukin-6 expression. Int J Cancer. 1993;55(1):96-101. doi: 10.1002/ijc.2910550118.
• 30. Pisa P, Halapi E, Pisa EK et al. Selective expression of interleukin 10, interferon gamma, and granulocyte-macrophage colony-stimulating factor in ovarian cancer biopsies. Proc Natl Acad Sci U S A. 1992;89(16):7708-7712. doi: 10.1073/pnas.89.16.7708.
• 31. Spits H, de Waal Malefyt R. Functional characterization of human IL-10. Int Arch Allergy Immunol. 1992;99(1):8-15. doi: 10.1159/000236329.
• 32. Eskdale J, Gallagher G. A polymorphic dinucleotide repeat in the human IL-10 promoter. Immunogenetics. 1995;42(5):444-445. doi: 10.1007/BF00179416.
• 33. Eskdale J, Kube D, Gallagher G. A second polymorphic dinucleotide repeat in the 5' flanking region of the human IL10 gene. Immunogenetics. 1996;45(1):82-83. doi: 10.1007/s002510050174.
• 34. Pandey M, Awasthi S, Singh U et al. Association of IL-10 Gene Polymorphism (-819C>T, -592C>A and -1082G>A) with Preterm Birth. Indian J Pediatr. 2018;85(2):93-101. doi: 10.1007/s12098-017-2496-9.
• 35. Al-shehmany AS, El-Kafoury AA., Haroun MA et al. Contribution of IL-10 (SNP -819 C/T and SNP-1082 G/A) polymorphisms variants to the risk of type 1 diabetes in Egyptian population. Iraqi Journal of Biotechnology. 2014;13(1):54-60.
• 36. Castelli V, Cimini A, Ferri C. Cytokine Storm in COVID-19: "When You Come Out of the Storm, You Won't Be the Same Person Who Walked in". Front Immunol. 2020;11:2132. doi: 10.3389/fimmu.2020.02132.
• 37. Lu L, Zhang H, Dauphars DJ et al. A Potential Role of Interleukin 10 in COVID-19 Pathogenesis. Trends Immunol. 2021;42(1):3-5. doi: 10.1016/j.it.2020.10.012.
• 38. Dhar SK, Vishnupriyan K, Damodar S et al. IL-6 and IL-10 as predictors of disease severity in COVID-19 patients: results from meta-analysis and regression. Heliyon. 2021;7(2):e06155. doi: 10.1016/j.heliyon.2021.e06155.
• 39. Zhao Y, Qin L, Zhang P et al. Longitudinal COVID-19 profiling associates IL-1RA and IL-10 with disease severity and RANTES with mild disease. JCI Insight. 2020;5(13):e139834. doi: 10.1172/jci.insight.139834.
• 40. Diao B, Wang C, Tan Y et al. Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19). Front Immunol. 2020;11:827. doi: 10.3389/fimmu.2020.00827.
• 41. Hu WC. Use interleukin-10 as the therapeutic agent for COVID-19. OSFPREPRINTS. 2020 doi: 10.31219/osf.io/arfhb.
• 42. Lu L, Zhang H, Zhan M et al. Preventing Mortality in COVID-19 Patients: Which Cytokine to Target in a Raging Storm? Front Cell Dev Biol. 2020;8:677. doi:10.3389/fcell.2020.00677.
• 43. Lauw FN, Pajkrt D, Hack CE et al. Proinflammatory effects of IL-10 during human endotoxemia. Journal of Immunology. 2000;165(5):2783-2789. doi: 10.4049/jimmunol.165.5.2783.
• 44. Li H, Liu L, Zhang D et al. SARS-CoV-2 and viral sepsis: observations and hypotheses. Lancet. 2020;395(10235):1517-1520. doi: 10.1016/S0140-6736(20)30920-X.
• 45. Potus F, Mai V, Lebret M et al. Novel insights on the pulmonary vascular consequences of COVID-19. Am J Physiol Lung Cell Mol Physiol. 2020;319(2):L277-L288. doi: 10.1152/ajplung.00195.2020.
• 46. Gattinoni L, Chiumello D, Caironi P et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med. 2020;46(6):1099-1102. doi: 10.1007/s00134-020-06033-2.
• 47. Song YG, Shin HS. COVID-19, A Clinical Syndrome Manifesting as Hypersensitivity Pneumonitis. Infect Chemother. 2020;52(1):110-112. doi: 10.3947/ic.2020.52.1.110.
• 48. Gattinoni L, Chiumello D, Rossi S. COVID-19 pneumonia: ARDS or not? Crit Care. 2020;24(1):154. doi: 10.1186/s13054-020-02880-z.
• 49. Conti P, Ronconi G, Caraffa A et al. Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by Coronavirus-19 (COVI-19 or SARS-CoV-2): anti-inflammatory strategies. J Biol Regul Homeost Agents. 2020;34(2):327-331. doi: 10.23812/CONTI-E.
• 50. Garg S, Garg M, Prabhakar N et al. Unraveling the mystery of Covid-19 cytokine storm: from skin to organ systems. Dermatologic Therapy. 2020;33:e13859. doi: 10.1111/dth.13859.
• 51. Ciceri F, Beretta L, Scandroglio AM et al. Microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome (MicroCLOTS): an atypical acute respiratory distress syndrome working hypothesis. Crit Care Resusc. 2020;22(2):95-97.
• 52. Cressoni M, Caironi P, Polli F et al. Anatomical and functional intrapulmonary shunt in acute respiratory distress syndrome. Crit Care Med. 2008;36(3):669-675. doi: 10.1097/01.CCM.0000300276.12074.E1.
• 53. Jain A, Doyle DJ. Stages or phenotypes? A critical look at COVID-19 pathophysiology. Intensive Care Med. 2020;46(7):1494-1495. doi: 10.1007/s00134-020-06083-6.
• 54. Gong MN, Thompson BT, Williams PL et al. Interleukin-10 polymorphism in position -1082 and acute respiratory distress syndrome. Eur Respir J. 2006;27(4):674-681. doi: 10.1183/09031936.06.00046405.
• 55. Turner DM, Williams DM, Sankaran D et al. An investigation of polymorphism in the interleukin-10 gene promoter. Eur J Immunogenet. 1997;24(1):1-8. doi: 10.1111/j.1365-2370.1997.tb00001.x.
• 56. Suárez A, Castro P, Alonso R, Mozo L, Gutiérrez C. Interindividual variations in constitutive interleukin-10 messenger RNA and protein levels and their association with genetic polymorphisms. Transplantation. 2003;75(5):711-717. doi: 10.1097/01.TP.0000055216.19866.9A.
• 57. Galley HF, Lowe PR, Carmichael RL et al. Genotype and interleukin-10 responses after cardiopulmonary bypass. Br J Anaesth. 2003;91(3):424-426. doi: 10.1093/bja/aeg174.
• 58. Gallagher PM, Lowe G, Fitzgerald T et al. Association of IL-10 polymorphism with severity of illness in community acquired pneumonia. Thorax. 2003;58(2):154-156. doi: 10.1136/thorax.58.2.154.
• 59. Schaaf BM, Boehmke F, Esnaashari H et al. Pneumococcal septic shock is associated with the interleukin-10-1082 gene promoter polymorphism. Am J Respir Crit Care Med. 2003;168(4):476-80. doi: 10.1164/rccm.200210-1164OC.
• 60. Ghafouri-Fard S, Noroozi R, Vafaee R et al. Effects of host genetic variations on response to, susceptibility and severity of respiratory infections. Biomed Pharmacother. 2020;128:110296. doi: 10.1016/j.biopha.2020.110296.