Role of Interferon Gamma in the Pathogenesis of Sickle Cell Crisis

Authors

  • Ahmed Mahmoud Khalifa Forensic and Toxicology Department, Faculty of Medicine, Ain-Shams University, Cairo, Egypt.
  • Bashair Mater Albeladi Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.
  • Hajar Abdulmalik Amin Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.
  • Nida Mahmoud Johari Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.
  • Rawan Sultan Alosaimi Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.
  • Wafa Ahmad Hamdi Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.`
  • Amal Fathy Gharib Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.
  • Howaida Mahmoud Hagag Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.
  • Asmaa Hassan Farghly Medical Laboratory Department, Faculty of Applied Medical Science, Taif University, Taif, Saudi Arabia.
  • Khadiga Ahmed Ismail Parasitology Department, Faculty of Medicine, Ain-Shams University, Cairo, Egypt.

Keywords:

Sickle cell disease, Crisis, Interferon gamma

Abstract

Sickle cell disease (SCD) is considered as one of the major public health disease worldwide. The high burden of the disease in Saudi Arabia and Egypt need more effort to control. Current evidence suggests that available care is suboptimal. Different types of crisis are considered significant complication of SCD, the pathogenesis of SCD is mainly due to the production of pro-inflammatory cytokines. As a result of the association of chronic inflammation with crisis onset and the role of IFN gamma as regulatory cytokines, we tested the association of level of IFN gamma with pathogenesis of sickle cell crisis. Study subjects comprised of 70 volunteers (42 (60%) males and 28 (40%)) and among 70 subjects, 50 were sickle cell patients [34 (48.6%) with stable condition, 16 (22.9%) with hemolytic crisis] and 20 (28.6%) healthy normal persons (Control group). Serum IFN gamma concentrations were determined by ELISA. It was found from the results that IFN gamma levels were significantly increased in both stable condition and hemolytic crisis patients in comparison to healthy normal control. There is a statistically significant increase in the level of interferon gamma in SCD patients with stable condition and in crisis in comparison to healthy control. Interferon gamma has a role in pathogenesis of inflammation in sickle cell individuals in the steady state or in crisis in comparison to healthy normal control.

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References

Modell B. Guidelines for the control of haemoglobin disorders. Sardinia, WHO, Italy, 1989.

Serjeant GR. Sickle-cell disease. The Lancet 1997; 350(9079): 725-730.

Modell B, Darlison M. Global epidemiology of haemoglobin disorders and derived service indicators. Bulletin of the World Health Organization 2008; 86(6): 480-487.

World Health Organisation 2008. Management of haemoglobin disorders. Proceedings of the Report of Joint WHO-TIF Meeting, Nicosia, Cyprus, 2007.

Piel FB, Patil AP, Howes RE, NyangiriOA, Gething PW, Dewi M, Temperley WH, Williams TN, Weatherall DJ, Hay SI. Global epidemiology of Sickle haemoglobin in neonates: a contemporary geostatistical model-based map and population estimates. The Lancet 2013; 381(9861): 142-151.

Jastaniah W. Epidemiology of sickle cell disease in Saudi Arabia. Annals of Saudi Medicine 2011; 31(3): 289-293.

Madigan C, Malik P. Pathophysiology and therapy for haemoglobinopathies; Part I: Sickle cell disease. Expert Reviews in Molecular Medicine 2006; 8(9): 1-23.

Makani J, Mgaya J, Balandya E, Msami K, Soka D, Cox SE, Komba AN, Rwezaula S, Meda E, Muturi D, Kitundu J, Fegan G, Kirkham F, Newton CR, Snow RW, Lowe B. Bacteraemia in sickle cell anaemia is associated with low haemoglobin: A report of 890 admissions to a tertiary hospital in Tanzania. British journal of haematology 2015; 171(2): 273-276.

Martinon F, Mayor A, Tschopp J. The inflammasomes: Guardians of the body. Annual Review of Immunology 2009; 27: 229-265.

Halle A, Hornung V, Petzold GC, Stewart CR, Monks BG, Reinheckel T, Fitzgerald KA, Latz E, Moore KJ, Golenbock DT. The NALP3 inflammasome is involved in the innate immune response to amyloid-beta. Nature Immunology 2008; 9(8): 857-865.

Martinon F, Burns K, Tschopp J. The inflammasome: A molecular platform triggering activation of inflammatory caspases and processing of proil-beta. Molecular Cell 2002; 10(2): 417-426.

Pathare A, Al Kindi S, Alnaqdy AA, Daar S, Knox Macaulay H, Dennison D. Cytokine profile of sickle cell disease in Oman. American Journal of Hematology 2004; 77(4): 323-328.

Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: A novel mechanism of human disease. JAMA 2005; 293(13): 1653-1662.

Vingert B, Tamagne M, Desmarets M, Pakdaman S, Elayeb R, Habibi A, Bernaudin F, Galacteros F, Bierling P, Noizat-Pirenne F, Cohen JL. Partial dysfunction of Treg activation in sickle cell disease. American journal of hematology 2014; 89(3): 261–266.

Machado PRL, Araújo MAS, Carvalho L, Carvalho EM. Mechanisms of immune response infections. Anais Brasileiro de Dermatologia 2004; 79(6): 647-662. 16. Janeway CA, Travers P, Walport M, Shlomchik M. Immunobiology. 5th Edition, Garland Publishing, New York, 2001.

Cetiner S, Akoglu TF, Kilinc Y, Akoglu E, Kumi M. Immunological studies in sickle cell disease: comparison of homozygote mild and severe variants. Clinical Immunology and Immunopathology 1989; 53(1): 32-39.

Mtatiro SN, Makani J, Mmbando B, Thein SL, Menzel S, Cox SE. Genetic variants at HbF-modifier loci moderate anemia and leukocytosis in sickle cell disease in Tanzania. American journal of hematology 2015; 90(1): 1-4.

Abbas AK, Lichtman AH, Pober JS. Celular and Molecular Immunology, Elsevier, USA, 2000.

Zhang D, Xu C, Manwani D, Frenette PS. Neutrophils, platelets, and inflammatory pathways at the nexus of sickle cell disease pathophysiology. Blood 2016; 127(7): 801-809.

Novelli EM, Gladwin MT. Crises in sickle cell disease. Chest 2016; 149(4): 1082-1093.

Zaini RG. Sickle-cell anemia and consanguinity among the Saudi Arabian population. Archives of Medicine 2016; 8(15): 1-3.

Alotaibi MM. Sickle cell disease in Saudi Arabia: A challenge or not. Journal of Epidemiology and Global Health 2017; 7(2): 99-101.

Ojo OT, Shokunbi WA, Ibijola AA, Arinola GA, Olatunji PO, Lasisi AO, Fayehun AF. Serum levels of Gamma-interferon and Interleukin-4 in homozygous sickle cell anaemia patients. International Blood Research & Reviews 2016; 5(2): 1-7.

Nnodim J, Meludu SC, Dioka CE, Martin I, Ukaibe N, Ihim A. Cytokine expression in homozygous SCA. Journal of Krishna Institute of Medical Science University 2015; 4(1):34-37.

Musa BOP, Onyemelukwe GC, Hambolu JO, Mamman AI, Albarka HI. Pattern of serum cytokine expression and T-cell subsets in Sickle Cell Disease patients in vaso-occlusive crisis. Clinical and Vaccine Immunology 2010; 17(4): 602-608.

Published

2018-07-07

How to Cite

Khalifa, A. M., B. M. Albeladi, H. A. Amin, N. M. Johari, R. S. Alosaimi, W. A. Hamdi, A. F. Gharib, H. M. . Hagag, A. H. Farghly, and K. A. Ismail. “Role of Interferon Gamma in the Pathogenesis of Sickle Cell Crisis”. UPI Journal of Pharmaceutical, Medical and Health Sciences, vol. 1, no. 2, July 2018, pp. 11-17, https://uniquepubinternational.com/journals/index.php/jpmhs/article/view/11.

Issue

Volume-1 Issue-2, 2018

Section

Research Articles(s)
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