Research Journal of Pharmacy and Technology

Open Access Open Access  Restricted Access Subscription Access
Open Access Open Access Open Access  Restricted Access Restricted Access Subscription Access

The Risk of Genetic Polymorphisms in the Immune Genes on the Developed of Respiratory Allergic Diseases


Affiliations
1 College of Science, Mustansiriyah University, Baghdad,, Iraq
     

   Subscribe/Renew Journal


Allergic diseases are intricate and improvement includes both natural and hereditary components. besides classic Tcell-originated T helper form-2 cytokine comparable to IL4; IL5; IL13. Tissues created cytokine akin to thymic-stromal-lymphopoietin. IL25 as well as IL33 at the moment is famous the main contribution of allergies irritation. IL33 generated via quite a lot of tissue living cells and generally enhances allergic infection using its results in hematopoietic-cells varieties. Ecological and endogenously triggered which induce IL33 cell released could also correlated to contamination, irritation and tissues harm. Current review brief an extensive variety for certified IL33 efficiency in human-cellular-mediatory in irritation like good as genetically marker when IL33 contributed with sickness. At last, IL33 attached with IL1/RL1 was engaged with asthma. previous information shows in some investigation that contribution by IL33-IL1RL1 gene with asthma was biologically conceivable, IL33 on asthma patients can influence expressing levels for IL33 serum. Moreover, rs16924159/G-A variation is related in IL33 level of respiratory hypersensitive diseases patients.

Keywords

Allergy, Polymorphism, IL33, Respiratory diseases, Iraq.
Subscription Login to verify subscription
User
Notifications
Font Size


  • Yazdanbakhsh M, Kremsner PG, van Ree R. Allergy, parasites, and the hygiene hypothesis. Science. 2002; 296 (5567): 490-494. doi:0.1126/science.296.5567.490.

  • Galli SJ, Tsai M, Piliponsky AM. The development of allergic inflammation. Nature. 2008; 454(7203): 445-454. doi:10.1038/nature07204

  • Kaur, G., Singh, A., Narang, R. K., and Singh, G. Asthma: From Disease to Treatment-An Overview. International Journal of Bio-Pharma Research. 2020; 9(4): 2651-2560.http://dx.doi.org/10.21746/ijbpr.2020.9.4.1

  • Small P, Keith PK, Kim H. Allergic rhinitis. Allergy Asthma Clinical Immunology. 2018; 14(Suppl 2): 51. doi:10.1186/s13223-018-0280-7

  • Son JH, Park SY, Cho YS, Chung BY, Kim HO, Park CW. Immediate Hypersensitivity Reactions Induced by Triamcinolone in a Patient with Atopic Dermatitis. Journal of Korean Medical Sciences. 2018; 33(12): e87. doi: 10.3346/jkms.2018.33.e87.

  • Koike Y, Sato S, Yanagida N, Asaumi T, Ogura K, Ohtani K, Imai T, Ebisawa M. Predictors of Persistent Milk Allergy in Children: A Retrospective Cohort Study. International Achieves of Allergy and Immunology. 2018; 175(3): 177-180. doi: 10.1159/000486311.

  • Martin NT, Martin MU. Interleukin 33 is a guardian of barriers and a local alarmin. Nature Immunology. 2016; 17(2): 122-131. doi: 10.1038/ni.3370. PMID: 26784265. 8. Cayrol C, Duval A, Schmitt P, Roga S, Camus M, et al.

  • Environmental allergens induce allergic inflammation through proteolytic maturation of IL-33. Nature Immunology, 2018; 19(4): 375-385. https://doi.org/10.1038/s41590-018-0067-5

  • Ding W, Zou GL, Zhang W, Lai XN, et al. Interleukin-33: its emerging role in allergic diseases. Molecules, 2018; 23(7): 1665. DOI:10.3390/molecules23071665

  • Chackerian AA, Oldham ER, Murphy EE, Schmitz J, Pflanz S, Kastelein RA. IL-1 receptor accessory protein and ST2 comprise the IL-33 receptor complex. The Journal of Immunology. 2007; 179(4): 2551-2555. doi: 10.4049/jimmunol.179.4.2551.

  • Gould HJ, Sutton BJ. IgE in allergy and asthma today. Nature. Reviews Immunology, 2008; 8: 205-217.https://doi.org/10.1038/nri2273

  • Stone KD, Prussin C, Metcalfe DD. IgE, mast cells, basophils and eosinophils. Journal Allergy Clinical immunology, 2010; 125(2 Suppl 2): S73-S80. doi:10.1016/j.jaci.2009.11.017

  • Yap JM, Ching MW, Cabanilla CQ, Ramos JD. Multiple house dust mite allergens sensitization profiles in children with allergic asthma. Journal of Allergy & Therapy, 2014; 5: 3. DOI:10.4172/2155-6121.1000179

  • Mansour AE, Yasein YA, Ghandour A, Zaidan O, Abo El-Abbas MM. Prevalence of bronchial asthma and its impact on the cognitive functions and academic achievement among preparatory school children in Egypt. The Journal of American Science, 2014; 10(7): 119-127.

  • Payrovee Z, Kashaninia Z, Rezasoltani P. Effect of family empowerment on the quality of life of school-aged children with asthma. Tanaffos, 2014; 13(1): 35-42.

  • Liu J, Shen JX, Hu LJ, Huang WH, Zhang GJ. Significance of interleukin -33 and its related cytokines in patient with breast cancer. Frontiers in Immunology, 2014; 5: 141.

  • Brightling CE, Gupta S, Gonem S, Siddiqui S. Lung damage and airway remodelling in severe asthma. Clinical and Experimental Allergy. 2012; 42(5): 638-649. doi: 10.1111/j.1365-2222.2011.03917.x.

  • Salujaa R, Ketelaarb ME, Hawroa T, et al. The role of the IL-33/IL-1RL1 axis in mast cell and basophil activation in allergic disorders. Molecular Immunology, 2015; 63(1): 80-85. doi: 10.1016/j.molimm.2014.06.018.

  • Solarski B, Kurowski M, Kewin P, Xu D, Liew FY. IL-33 exacerbates eosinophil-mediated airway inflammation. Journal Immunology, 2010; 185(6): 3472-3480. doi: 10.4049/jimmunol.1000730.

  • Lu J, Kang J, Zhang C, Zhang X. The role of IL-33/ST2L signals in immune cells. Immunology Letters, 2015; 164(1): 11-17. doi: 10.1016/j.imlet.2015.01.008.

  • Kreutzfeldt M, Hegazy AN, Schrick G, Fallon PG, Klemenz R. The alarmin interleukin-33 drives protective antiviral CD8+ T cell response. Science, 2012; 335(6071): 984-989. doi: 10.1038/nature13577.

  • Villarreal DO, Weiner.B. Interleukin-33: A switch-hitting cytokine. Current Opinion in Immunology, 2014; 28: 102-106. doi: 10.1016/j.coi.2014.03.004.

  • Herbert C, Bunting MM, Lambie N, Thomas PS, Kumar RK. Immunoreactivity for interleukin-33 in allergic airway inflammation. Journal Cytology & Histology, 2015; 6: 1. http://dx.doi.org/10.4172/2157-7099.1000302

  • Lamkanfi M, Dixit VM. IL-33 raises alarm. Immunity, 2009; 31(1): 5-7. doi: 10.1016/j.immuni.2009.06.011.

  • Makrinioti H, Toussaint M, Jackson DJ, Walton RP, Johnston SL. Role of IL-33 in respiratory allergy and asthma. The Lancet Respiratory Medicine, 2014; 2(3): 226-237. doi: 10.1016/S2213-2600(13)70261-3.

  • Farahani R, Sherkat R, Hakemi MG, Eskandari N, Yazdani R. Cytokine (interleukin-9, IL-17, IL-22, IL25 and IL-33) and asthma. Advanced Biomedical Research, 2014; 3: 127. doi:10.4103/2277-9175.133249

  • Liew FY, Pitman NI, Mcinnes IB. Disease-associated functions of IL-33: The new kid in the IL-1 family. Nature Reviews Immunology, 2010; 10: 103-110.

  • Borish L, Steinke JW. Interleukin -33 in asthma: How big of role does it play? Current Allergy and Asthma Reports, 2011; 11(1): 7-11.

  • Lioyd CM. IL-33-family members in asthma bringing innate and adaptive immune responses. Current Opinion in Immunology, 2010; 22(6): 800-806. doi: 10.1016/j.coi.2010.10.006.

  • Xu WD, Zhang M, Zhang YJ, Ye DQ. IL-33 in rheumatoid arthritis: Potential role in pathogenesis and therapy. Human Immunology, 2013; 74(9): 1057-1060. doi: 10.1016/j.humimm.2013.06.029.

  • Sattler S, Smits HH, Xu D, Huang FP. The evolutionary role of the IL-33/ST2 system in host immune defence. Archivum Immunologiae Therapiae Experimentalis, 2013; 61: 107-117. doi: 10.1007/s00005-012-0208-8.

  • Lloyd M. Allergy investigation: Major irritation or minor aggravation. In: Pathology Forum, 1st ed, 2014; 4: 6-8.

  • Sakashita M, Yoshimoto T, Hirota T, Harada M.; et al. Association of serum interleukin-22 level and the interleukin-33 genetic variant with Japanese cedar pollinosis. Clinical Experimental Allergy, 2008; 38: 1875-1881. doi: 10.1111/j.1365-2222.2008.03114.x.

  • Haenuki Y, Matsushita K, Futatsugi S. A critical role of IL-33 in experimental allergic rhinitis. Journal Allergy Clinical Immunology, 2012; 130: 184-194. doi: 10.1016/j.jaci.2012.02.013.

  • Azizy EA, Elshora AE, Tantawy EA, Elsayd MA. Serum levels of interleukin-33 and its soluble receptor ST2 in asthmatic patients. Egyptian Journal of Chest Diseases and Tuberculosis, 2014; 63: 279-284. https://doi.org/10.1016/j.ejcdt.2013.11.005

  • Prefontaine D, Nadige J, Chouiali F, Audusseau S, et al. Increased IL-33 expression by epithelial cells in bronchial asthma. Journal Allergy Clinical Immunology, 2010; 125: 752-754. doi: 10.1016/j.jaci.2009.12.935.

  • Guo Z, Wu J, Zhao J, Lin F, Chen Y, Bi L, et al. IL33 promotes airway remodeling and is a marker of asthma disease severity. Journal Asthma, 2014; 5: 1-7. doi: 10.3109/02770903.2014.921196.

  • Asaka D, Yoshikawa M, Nakayama T, Yoshimura T, et al. Elevated levels of interleukin-33 in the nasal secretions of patients with allergic rhinitis. International Archives of Allergy and Immunology, 2012; 158(Supp 1): 47-50. doi: 10.1159/000337764.

  • Gluck J, Rymanczyk B, Rogala B. Serum IL33 but not ST2 level is elevated in intermittent allergic rhinitis and is a marker of disease severity. Inflammation Research Journal, 2012; 61(6): 547-550. doi: 10.1007/s00011-012-0443-9.

  • Ramdan MI, Candra P, K, Lusiana D, Duma K. Redesign of the Traditional Handloom for Sarong Female-Weavers Based on Anthropometric Data. 2020.

  • Moussion C, Ortega N, Girard JP. The IL-1-like cytokine IL-33 is constitutively expressed in the nucleus of endothelial cells and epithelial cells in vivo: a novel ‘alarmin’?. PloS one, 2008; 3(10): e3331. doi: 10.1371/journal.pone.0003331.

  • Gao X, Chi, X., Wang, X., Wu, R., Xu, H., et al.IL-33 Inhibits Hepatitis B Virus through Its Receptor ST2 in Hydrodynamic HBV Mouse Model. Mediators of Inflammation, 2020.

  • Mizutani N, Nabe T, Yoshino S. Interleukin‐33 and alveolar macrophages contribute to the mechanisms underlying the exacerbation of IgE‐mediated airway inflammation and remodelling in mice. Immunology, 2013; 139(2): 205-218. doi: 10.1111/imm.12071.

  • Kim S, Forno E, Yan Q, Jiang Y, et al. SNPs identified by GWAS affect asthma risk through DNA methylation and expression of cis-genes in airway epithelium. European Respiratory Journal, 2020; 55(4): 1902079. doi: 10.1183/13993003.02079-2019.

  • Queiroz GDA, Costa RDS, Alcantara‐Neves NM, et al. IL33 and IL1RL1 variants are associated with asthma and atopy in a Brazilian population. International Journal of Immunogenetics, 2017; 44(2): 51-61. doi: 10.1111/iji.12306.

  • Chen J, Zhang J, Hu H, Jin Y, Xue M. Polymorphisms of RAD50, IL33 and IL1RL1 are associated with atopic asthma in Chinese population. Tissue Antigens, 2015; 86(6): 443-447. doi: 10.1111/tan.12688.

  • Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduction and Targeted Therapy, 2017; 2(1): 1-9. https://doi.org/10.1038/sigtrans.2017.23

  • Yuliwulandari R, Kashiwase K, Nakajima H, Uddin J, et al. Polymorphisms of HLA genes in Western Javanese (Indonesia): close affinities to Southeast Asian populations. Tissue Antigens, 2009; 73(1): 46-53. doi: 10.1111/j.1399-0039.2008.01178.x.

  • Baranzehi T, Karimi-Davani S, Kordi-Tamandani DM. Analysis of IL-33 Gene Polymorphisms (rs1157505C/G and rs11792633C/T) and the Risk of Tuberculosis in South[t45eastern Iran. Journal of Genetic Research. 2020; 6(1): 54-59. DOI: 10.22080/jgr.2020.17777.1166

  • Smith DE. IL‐33: a tissue derived cytokine pathway involved in allergic inflammation and asthma. Clinical & Experimental Allergy, 2010; 40(2): 200-208. doi: 10.1111/j.1365-2222.2009.03384.x.

  • Hamzah IH, Ali Shafi FA, Noor Al-Huda AAHS. Study the Association of CYP3A5 Polymorphism on the Risk of Breast Cancer in Some of the Iraqi Women. Journal of Global Pharma Technology| 2018; 10(08):325-330

  • HamzahIH, Ali Shafi FA, Al Sharqi SAH, Brakhas SA. Cytology and molecular study for GSTP1 effect on asthma Iraqi patients. Clin Mol Allergy. 2019; 17: 4. https://doi.org/10.1186/s12948-019-0108-0

  • Saeed NAAA, Hamzah IH, Mohammed Ali AN, Abuderman ABA. Prediction of single nucleotide polymorphisms (SNPs) in apolipoprotein E gene and their possible associations with a deleterious effect on the structure and functional properties: an in silico approach. Network Modeling Analysis in Health Informatics and Bioinformatics. 2018; 7: 16. https://doi.org/10.1007/s13721-018-0178-9


Abstract Views: 147

PDF Views: 0




  • The Risk of Genetic Polymorphisms in the Immune Genes on the Developed of Respiratory Allergic Diseases

Abstract Views: 147  |  PDF Views: 0

Authors

Noor Al-Huda Ali A. H. Saeed
College of Science, Mustansiriyah University, Baghdad,, Iraq
Alaa N Mohammed Ali
College of Science, Mustansiriyah University, Baghdad,, Iraq
Israa Hussein Hamzah
College of Science, Mustansiriyah University, Baghdad,, Iraq

Abstract


Allergic diseases are intricate and improvement includes both natural and hereditary components. besides classic Tcell-originated T helper form-2 cytokine comparable to IL4; IL5; IL13. Tissues created cytokine akin to thymic-stromal-lymphopoietin. IL25 as well as IL33 at the moment is famous the main contribution of allergies irritation. IL33 generated via quite a lot of tissue living cells and generally enhances allergic infection using its results in hematopoietic-cells varieties. Ecological and endogenously triggered which induce IL33 cell released could also correlated to contamination, irritation and tissues harm. Current review brief an extensive variety for certified IL33 efficiency in human-cellular-mediatory in irritation like good as genetically marker when IL33 contributed with sickness. At last, IL33 attached with IL1/RL1 was engaged with asthma. previous information shows in some investigation that contribution by IL33-IL1RL1 gene with asthma was biologically conceivable, IL33 on asthma patients can influence expressing levels for IL33 serum. Moreover, rs16924159/G-A variation is related in IL33 level of respiratory hypersensitive diseases patients.

Keywords


Allergy, Polymorphism, IL33, Respiratory diseases, Iraq.

References