Document Type : Original Article

Authors

1 Department of Medical Biochemistry, Faculty of Medicine, Zabol University of Medical Sciences, Zabol, Iran

2 Department of Maternal Fetal Medicine, Zabol Medicinal Plants Research Center, Zabol University of Medical Sciences Zabol, Iran

3 Department of Internal Medicine, School of Medicine, Amir al momenin Hospital, Zabol University of Medical Sciences, Zabol, Iran

4 Forensic medicine and toxicology, Zabol University of medical sciences, Zabol, Iran.

5 Department of Microbiology, Medical Faculty- Zabol University of Medical Sciences, Zabol, Iran

10.55705/cmbr.2021.356674.1059

Abstract

The DNA polymorphisms found in clinical strains of Mycobacterium tuberculosis drive altered physiology, virulence, and pathogenesis in them. This study aimed to investigate the association between IL23R 1142 G/A (Arg381Gln) and GM-CSF 3928 C/T (Ile117Thr) gene polymorphisms with the incidence rate of tuberculosis in the population of Sistan. This study was based on the descriptive and applied type. All patients with active pulmonary tuberculosis were referred to the tuberculosis center of Zabol city for one year, with an equal number of healthy people adapted to the patients examined in terms of age. After data collecting to compare the frequency of polymorphisms, the chi-square test and OR index were used using SPSS software version 16. We have found that the IL23R reduced-function allele 1142A and genotypes CC and TC were overrepresented, especially in the Pad subgroup compared with the control group (44% versus 42%, 21% versus 22%, and 44% versus 39%, respectively. Increased risks of TB with minimal/moderate lung involvement, respectively. Our results demonstrate that the reduced-function polymorphism 1142G ¡ A encoded by IL23R influences the outcome of disease severity of active pulmonary TB in ZABOL patients. The genotypic and allelic frequency of IL23R 1142 G/A, and GM-CSF 3928 C/T (Ile117Thr) polymorphism in patients with tuberculosis was significantly different from the control group and this polymorphism was associated with the incidence of tuberculosis in the population of Sistan.

Graphical Abstract

The relationship between IL23R 1142G / A (Arg381Gln) and GM-CSF 3928 C / T (Ile117Thr) gene polymorphism in Iranian patients with tuberculosis disease

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ِDr. Khadije Rezaie Keikhaie
Zabol University of Medical Sciences

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  1. Luo Y, Xue Y, Song H, Tang G, Liu W, Bai H, Yuan X, Tong S, Wang F, Cai Y, Sun Z (2022) Machine learning based on routine laboratory indicators promoting the discrimination between active tuberculosis and latent tuberculosis infection. Journal of Infection 84(5):648-657. doi:https://doi.org/10.1016/j.jinf.2021.12.046
  2. Xin H, Zhang H, Yang S, Liu J, Lu W, Bai L, Cao X, Feng B, Jin Q, Gao L (2019) 5-Year Follow-up of Active Tuberculosis Development From Latent Infection in Rural China. Clinical Infectious Diseases 70(5):947-950. doi:https://doi.org/10.1093/cid/ciz581
  3. Ghadimi D, de Vrese M, Heller KJ, Schrezenmeir J (2010) Lactic acid bacteria enhance autophagic ability of mononuclear phagocytes by increasing Th1 autophagy-promoting cytokine (IFN-γ) and nitric oxide (NO) levels and reducing Th2 autophagy-restraining cytokines (IL-4 and IL-13) in response to Mycobacterium tuberculosis antigen. International Immunopharmacology 10(6):694-706. doi:https://doi.org/10.1016/j.intimp.2010.03.014
  4. Roetzer A, Diel R, Kohl TA, Rückert C, Nübel U, Blom J, Wirth T, Jaenicke S, Schuback S, Rüsch-Gerdes S, Supply P, Kalinowski J, Niemann S (2013) Whole Genome Sequencing versus Traditional Genotyping for Investigation of a Mycobacterium tuberculosis Outbreak: A Longitudinal Molecular Epidemiological Study. PLOS Medicine 10(2):e1001387. doi:https://doi.org/10.1371/journal.pmed.1001387
  5. Feo F, De Miglio MR, Simile MM, Muroni MR, Calvisi DF, Frau M, Pascale RM (2006) Hepatocellular carcinoma as a complex polygenic disease. Interpretive analysis of recent developments on genetic predisposition. Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1765(2):126-147. doi:https://doi.org/10.1016/j.bbcan.2005.08.007
  6. Cohen T, Helden PDv, Wilson D, Colijn C, McLaughlin MM, Abubakar I, Warren RM (2012) Mixed-Strain Mycobacterium tuberculosis Infections and the Implications for Tuberculosis Treatment and Control. Clinical Microbiology Reviews 25(4):708-719. doi:https://doi.org/10.1128/CMR.00021-12
  7. Divangahi M, Khan N, Kaufmann E (2018) Beyond Killing Mycobacterium tuberculosis: Disease Tolerance. Frontiers in Immunology 9. doi:https://doi.org/10.3389/fimmu.2018.02976
  8. Zhao ZZ, Savage NW, Sugerman PB, Walsh LJ (2002) Mast cell/T cell interactions in oral lichen planus. Journal of Oral Pathology & Medicine 31(4):189-195. doi:https://doi.org/10.1034/j.1600-0714.2002.310401.x
  9. Ramon-Luing LA, Carranza C, Téllez-Navarrete NA, Medina-Quero K, Gonzalez Y, Torres M, Chavez-Galan L (2022) Mycobacterium tuberculosis H37Rv Strain Increases the Frequency of CD3+TCR+ Macrophages and Affects Their Phenotype, but Not Their Migration Ability. International Journal of Molecular Sciences 23(1):329
  10. Choreño Parra JA, Martínez Zúñiga N, Jiménez Zamudio LA, Jiménez Álvarez LA, Salinas Lara C, Zúñiga J (2017) Memory of Natural Killer Cells: A New Chance against Mycobacterium tuberculosis? Frontiers in Immunology 8. doi:https://doi.org/10.3389/fimmu.2017.00967
  11. Ogongo P, Tezera LB, Ardain A, Nhamoyebonde S, Ramsuran D, Singh A, Ng’oepe A, Karim F, Naidoo T, Khan K, Dullabh KJ, Fehlings M, Lee BH, Nardin A, Lindestam Arlehamn CS, Sette A, Behar SM, Steyn AJC, Madansein R, Kløverpris HN, Elkington PT, Leslie A (2021) Tissue-resident-like CD4+ T cells secreting IL-17 control Mycobacterium tuberculosis in the human lung. The Journal of Clinical Investigation 131(10). doi:https://doi.org/10.1172/JCI142014
  12. Damiani G, McCormick TS, Leal LO, Ghannoum MA (2020) Recombinant human granulocyte macrophage-colony stimulating factor expressed in yeast (sargramostim): A potential ally to combat serious infections. Clinical Immunology 210:108292. doi:https://doi.org/10.1016/j.clim.2019.108292
  13. Puttur F, Gregory LG, Lloyd CM (2019) Airway macrophages as the guardians of tissue repair in the lung. Immunology & Cell Biology 97(3):246-257. doi:https://doi.org/10.1111/imcb.12235
  14. Carey B, Trapnell BC (2010) The molecular basis of pulmonary alveolar proteinosis. Clinical Immunology 135(2):223-235. doi:https://doi.org/10.1016/j.clim.2010.02.017
  15. Mishra A, Singh VK, Jagannath C, Subbian S, Restrepo BI, Gauduin MC, Khan A (2022) Human Macrophages Exhibit GM-CSF Dependent Restriction of Mycobacterium tuberculosis Infection via Regulating Their Self-Survival, Differentiation and Metabolism. Front Immunol 13:859116. doi:https://doi.org/10.3389/fimmu.2022.859116
  16. Ehlers S, Schaible U (2013) The Granuloma in Tuberculosis: Dynamics of a Host–Pathogen Collusion. Frontiers in Immunology 3. doi:https://doi.org/10.3389/fimmu.2012.00411
  17. Kopf M, Schneider C, Nobs SP (2015) The development and function of lung-resident macrophages and dendritic cells. Nature Immunology 16(1):36-44. doi:https://doi.org/10.1038/ni.3052
  18. Baharom F, Rankin G, Blomberg A, Smed-Sörensen A (2017) Human Lung Mononuclear Phagocytes in Health and Disease. Frontiers in Immunology 8. doi:https://doi.org/10.3389/fimmu.2017.00499
  19. Rolandelli A, Pellegrini JM, Hernández Del Pino RE, Tateosian NL, Amiano NO, Morelli MP, Castello FA, Casco N, Levi A, Palmero DJ, García VE (2019) The Non-synonymous rs763780 Single-Nucleotide Polymorphism in IL17F Gene Is Associated With Susceptibility to Tuberculosis and Advanced Disease Severity in Argentina. Frontiers in Immunology 10. doi:https://doi.org/10.3389/fimmu.2019.02248
  20. Scheller J, Berg A, Moll JM, Floss DM, Jungesblut C (2021) Current status and relevance of single nucleotide polymorphisms in IL-6-/IL-12-type cytokine receptors. Cytokine 148:155550. doi:https://doi.org/10.1016/j.cyto.2021.155550
  21. Lewinsohn DM, Leonard MK, LoBue PA, Cohn DL, Daley CL, Desmond E, Keane J, Lewinsohn DA, Loeffler AM, Mazurek GH, O’Brien RJ, Pai M, Richeldi L, Salfinger M, Shinnick TM, Sterling TR, Warshauer DM, Woods GL (2017) Official American Thoracic Society/Infectious Diseases Society of America/Centers for Disease Control and Prevention Clinical Practice Guidelines: Diagnosis of Tuberculosis in Adults and Children. Clinical Infectious Diseases 64(2):e1-e33. doi:https://doi.org/10.1093/cid/ciw694
  22. American Thoracic S (2000) Diagnostic standards and classification of tuberculosis in adults and children. Am J Respir Crit Care Med 161:1376-1395. doi:https://doi.org/1571417124337616000
  23. Zakeri S, Pirahmadi S, Mehrizi AA, Djadid ND (2011) Genetic variation of TLR-4, TLR-9 and TIRAP genes in Iranian malaria patients. Malaria Journal 10(1):77. doi:https://doi.org/10.1186/1475-2875-10-77
  24. Bafica A, Scanga CA, Feng CG, Leifer C, Cheever A, Sher A (2005) TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis. Journal of Experimental Medicine 202(12):1715-1724. doi:https://doi.org/10.1084/jem.20051782
  25. Kuai S-G, Ou Q-F, You D-H, Shang Z-B, Wang J, Liu J, Zhou X-K, Pei H, Huang L-H (2016) Functional polymorphisms in the gene encoding macrophage migration inhibitory factor (MIF) are associated with active pulmonary tuberculosis. Infectious Diseases 48(3):222-228. doi:https://doi.org/10.3109/23744235.2015.1107188
  26. Jiang D, Wubuli A, Hu X, Ikramullah S, Maimaiti A, Zhang W, Wushouer Q (2015) The variations of IL-23R are associated with susceptibility and severe clinical forms of pulmonary tuberculosis in Chinese Uygurs. BMC Infectious Diseases 15(1):550. doi:https://doi.org/10.1186/s12879-015-1284-2
  27. Abdelaal EB, Abdelsamie HM, Attia SM, Amr KS, Eldahshan RM, Elsaie ML (2021) Association of a novel Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)-3928C/T and GM-CSF(3606T⁄C) Promoter gene polymorphisms with the pathogenesis and severity of acne vulgaris: A case-controlled study. Journal of Cosmetic Dermatology 20(11):3679-3683. doi:https://doi.org/10.1111/jocd.14481
  28. Robinson RT (2017) T Cell Production of GM-CSF Protects the Host during Experimental Tuberculosis. mBio 8(6):e02087-02017. doi:https://doi.org/10.1128/mBio.02087-17
  29. Saeki H, Tsunemi Y, Asano N, Nakamura K, Sekiya T, Hirai K, Kakinuma T, Fujita H, Kagami S, Tamaki K (2006) Analysis of GM-CSF gene polymorphisms (3606T/C and 3928C/T) in Japanese patients with atopic dermatitis. Clinical and Experimental Dermatology 31(2):278-280. doi:https://doi.org/10.1111/j.1365-2230.2005.02052.x