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Mohammed H Al-Mquter, L. F, Abdul Azeez Atiayh, S. (1402). Evaluation of IL-6, IL-25 & IL-35 in the COVID 19 Patients and their Correlation to Demography Data in the Symptomatic Patients. سامانه مدیریت نشریات علمی, 78(3), 1049-1056. doi: 10.22092/ari.2022.360087.2547
L. F Mohammed H Al-Mquter; S Abdul Azeez Atiayh. "Evaluation of IL-6, IL-25 & IL-35 in the COVID 19 Patients and their Correlation to Demography Data in the Symptomatic Patients". سامانه مدیریت نشریات علمی, 78, 3, 1402, 1049-1056. doi: 10.22092/ari.2022.360087.2547
Mohammed H Al-Mquter, L. F, Abdul Azeez Atiayh, S. (1402). 'Evaluation of IL-6, IL-25 & IL-35 in the COVID 19 Patients and their Correlation to Demography Data in the Symptomatic Patients', سامانه مدیریت نشریات علمی, 78(3), pp. 1049-1056. doi: 10.22092/ari.2022.360087.2547
Mohammed H Al-Mquter, L. F, Abdul Azeez Atiayh, S. Evaluation of IL-6, IL-25 & IL-35 in the COVID 19 Patients and their Correlation to Demography Data in the Symptomatic Patients. سامانه مدیریت نشریات علمی, 1402; 78(3): 1049-1056. doi: 10.22092/ari.2022.360087.2547

Evaluation of IL-6, IL-25 & IL-35 in the COVID 19 Patients and their Correlation to Demography Data in the Symptomatic Patients

Archives of Razi Institute
مقاله 34، دوره 78، شماره 3، مرداد و شهریور 2023، صفحه 1049-1056    اصل مقاله (552.78 K)
نوع مقاله: Original Articles
شناسه دیجیتال (DOI): 10.22092/ari.2022.360087.2547
نویسندگان
L. F Mohammed H Al-Mquter* 1؛ S Abdul Azeez Atiayh2
1Microbiology Department, College of Medicine, University of Thi-Qar, Nasiriyah, Iraq
2Microbiology Department, Cancer Research Unit, College of Medicine, University of Thi-Qar, Nasiriyah, Iraq
چکیده
The severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, was first discovered in Wuhan, Hubei province, China. Cytokines play a critical role in COVID-19 infections through their inflammatory or anti-inflammatory activities. This study aimed to detect the diagnostic value of and the relationship between the interleukins under study, in addition to their relationship with demographic data in COVID-19 patients. Patients with a confirmed diagnosis of COVID-19 based on laboratory (PCR) results and the healthy control group were given their section of this investigation. The patient group had 120 COVID-19 patients, including 62 males and 58 females, while the control group consisted of 32 individuals (22 males and 10 females). The subdivision was then performed according to their vaccination status, chronic diseases, gender, and residence. Cytokine levels were detected using the ELISA technique. The immunological status of COVID-19 patients was determined by measuring interleukin (IL)-6, IL-25, and IL-35. During the research, it was found that IL-6 was highly significant in COVID-19 patients (0.001). However, its level was not significantly different (0.376) in patients regarding the type of chronic diseases, residence (0.353), and gender (0.574), but it was significantly different in vaccinated patients (0.029). It was also found that IL-6 is significantly correlated with IL-25 and IL-35. IL-25 was highly significant in COVID-19 patients (0.007), and there was a significant difference in its level in patients regarding the type of chronic disease (0.049). While there was no difference in terms of residence (0.421) and gender (0.681), corona vaccination showed a significant difference (0.047). IL-25 also had a significant correlation with IL-6 and IL-35. As for IL-35, it was significant in patients with COVID-19 (0.013) but not significantly different regarding chronic diseases (0.344), residence (0.877), or gender (0.800). However, it was significantly different in vaccinated patients, compared to the non-vaccinated ones. IL-35 was found to be significantly correlated with IL-25 and IL-6 (0.000). The examined interleukins increased in COVID-19 individuals. IL-6 remains an excellent marker for determining the immune state of patients with COVID-19. There were also strong correlations between the interleukins under study in COVID-19 patients. However, there was no relationship between age, residence, gender, and the concentration of studied cytokines. IL-25 increases significantly in COVID-19 patients suffering from chronic diseases. Therefore, it is more efficient in the follow-up of patients.
کلیدواژه‌ها
Cytokines؛ Interleukins؛ SARS-CoV-2
سایر فایل های مرتبط با مقاله
مراجع
  1. Singhal T. Review on COVID19 disease so far. Indian J Pediatr. 2020;87(4):281-6.
  2. Jernigan DB, COVID C, Team R. Update: public health response to the coronavirus disease 2019 outbreak—United States, February 24, 2020. Morb Mortal Wkly Rept. 2020;69(8):216.
  3. Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen 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):271-80.
  4. Ferguson-Smith AC, Chen Y-F, Newman MS, May LT, Sehgal PB, Ruddle FH. Regional localization of the interferon-β2B-cell stimulatory factor 2/hepatocyte stimulating factor gene to human chromosome 7p15-p21. Genomics. 1988;2(3):203-8.
  5. Febbraio MA, Pedersen BK. Contraction-induced myokine production and release: is skeletal muscle an endocrine organ? Exerc Sport Sci Rev. 2005;33(3):114-9.
  6. Moseley T, Haudenschild DR, Rose L, Reddi AH. Interleukin-17 family and IL-17 receptors. Cytokine Growth Factor Rev. 2003;14(2):155-74.
  7. Lee J, Ho W-H, Maruoka M, Corpuz RT, Baldwin DT, Foster JS, et al. IL-17E, a novel proinflammatory ligand for the IL-17 receptor homolog IL-17Rh1. J Biol Chem. 2001;276(2):1660-4.
  8. Behzadi P, Behzadi E, Ranjbar R. IL-12 family cytokines: general characteristics, pathogenic microorganisms, receptors, and signalling pathways. Acta Microbiol Immunol Hung. 2016;63(1):1-25.
  9. Li X, Shao Y, Sha X, Fang P, Kuo Y-M, Andrews AJ, et al. IL-35 (interleukin-35) suppresses endothelial cell activation by inhibiting mitochondrial reactive oxygen species-mediated site-specific acetylation of H3K14 (histone 3 lysine 14). Arterioscler Thromb Vasc Biol. 2018;38(3):599-609.
  10. Li X, Mai J, Virtue A, Yin Y, Gong R, Sha X, et al. IL-35 is a novel responsive anti-inflammatory cytokine—a new system of categorizing anti-inflammatory cytokines. PloS One. 2012;7(3):e33628.
  11. Pedersen SF, Ho Y-C. SARS-CoV-2: a storm is raging. J Clin Invest. 2020;130(5):2202-5.
  12. McGonagle D, Sharif K, O'Regan A, Bridgewood C. The role of cytokines including interleukin-6 in COVID-19 induced pneumonia and macrophage activation syndrome-like disease. Autoimmun Rev. 2020:19(6):102537.
  13. Yuki K, Fujiogi M, Koutsogiannaki S. COVID-19 pathophysiology: A review. Clin Immunol. 2020;215:108427.
  14. hu H, Shuai H, Hou Y, Zhang X, Wen L, Huang X, et al. Targeting highly pathogenic coronavirus-induced apoptosis reduces viral pathogenesis and disease severity. Sci Adv. 2021;7(25):eabf8577.
  15. Barlow JL, McKenzie AN. Nuocytes: expanding the innate cell repertoire in type‐2 immunity. J Leukoc Biol. 2011;90(5):867-74.
  1. Goossens N, Nakagawa S, Sun X, Hoshida Y. Cancer biomarker discovery and validation. Transl Cancer Res. 2015;4(3):256.
  2. Turnis ME, Sawant DV, Szymczak-Workman AL, Andrews LP, Delgoffe GM, Yano H, et al. Interleukin-35 limits anti-tumor immunity. Immunity. 2016;44(2):316-29
  3. Zeng J-C, Zhang Z, Li T-Y, Liang Y-F, Wang H-M, Bao J-J, et al. Assessing the role of IL-35 in colorectal cancer progression and prognosis. Int J Clin Exp Pathol. 2013;6(9):1806.
  4. Choi J, Leung PS, Bowlus C, Gershwin ME. IL-35 and autoimmunity: a comprehensive perspective. Clin Rev Allergy Immunol. 2015;49(3):327-32.
  5. Li X, Tian L, Dong Y, Zhu Q, Wang Y, Han W, et al. IL-35 inhibits HBV antigen-specific IFN-γ-producing CTLs in vitro. Clin Sci. 2015;129(5):395-404.
  6. Htun NSN, Odermatt P, Eze IC, Boillat-Blanco N, D’Acremont V, Probst-Hensch N. Is diabetes a risk factor for a severe clinical presentation of dengue?-review and meta-analysis. PLoS Negl Trop Dis. 2015;9(4):e0003741.
  7. Incalza MA, D'Oria R, Natalicchio A, Perrini S, Laviola L, Giorgino F. Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases. Vascul Pharmacol. 2018;100:1-9.
  8. Han H, Yang L, Liu R, Liu F, Wu K-l, Li J, et al. Prominent changes in blood coagulation of patients with SARS-CoV-2 infection. Clin Chem Lab Med. 2020;58(7):1116-20.
  9. Zinkernagel RM. On natural and artificial vaccinations. Annu Rev Immunol. 2003;21:515.
  10. Grifoni A, Weiskopf D, Ramirez SI, Mateus J, Dan JM, Moderbacher CR, et al. Targets of T cell responses to SARS-CoV-2 coronavirus in humans with COVID-19 disease and unexposed individuals. Cell. 2020;181(7):1489-501.
  11. Shrotri M, van Schalkwyk MC, Post N, Eddy D, Huntley C, Leeman D, et al. T cell response to SARS-CoV-2 infection in humans: A systematic review. PloS One. 2021;16(1):e0245532.
  12. Dong J, Wong C, Cai Z, Jiao D, Chu M, Lam C. Amelioration of allergic airway inflammation in mice by regulatory IL‐35 through dampening inflammatory dendritic cells. Allergy. 2015;70(8):921-32.
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