Eurasian Journal of Biosciences

Role of interleukin 25 and interleukin 33 as immunological markers in pediatric asthma
  • Article Type: Research Article
  • Eurasian Journal of Biosciences, 2020 - Volume 14 Issue 2, pp. 4625-4630
  • Published Online: 30 Oct 2020
  • Open Access Full Text (PDF)


Background: Asthma is a chronic airways disease recognized by variable obstruction of the airflow, airway inflammation and hypperesponsiveness of the airway. The epithelial cytokines IL-33 and IL-25 have been implicated in asthma pathogenesis because they promote Th2-type cytokine synthesis.
Objectives: This study amid to show the role of both interleukins 25 and 33 in the airway inflammation.
Methods: The case- control study included 74 asthmatic children as patients group, 75 non asthmatic children as control group. Serum levels of IL-25 and IL-33 was measured by sandwich ELISA using ELISA kit (CUSABIO-china).
Results: Asthma was reported in a high frequency among males 56 (75.7%) than females 18 (24.3%). There was a high frequency of family history of asthma 50 (67.6%) and rhinitis 58(78.4%) in asthmatic patients. Also, there were a high frequency of aggravating by flu 50 (67.6 %) and dust 40 (54.1%) in asthmatic patients. According to the treatment, there was a high frequency of montelukaste 30 (40.5%) in asthmatic patients. In addition, there was a high frequency of mild severity in asthmatic patients. The serum level of IL-25 have a highly significant (P= 0.000) association with susceptibility to asthma, while IL-33 showing a non-significant (P= 0.473) association with the disease. Also, there were a non- significant correlation (P= 0.688) between IL-25 and IL-33 with the disease. Regarding correlation of IL-25 and IL-33 with Immunoglobulin E and eosinophil's count showing a non-significant association in asthmatic patients.
Conclusion: There was a highly significant association between the IL-25 serum level and susceptibility to asthma. Also, this study was reported a non-significant relationship between IL-33 and asthmatic disease.


  • Barlow J L, Peel S, Fox J, Panova V, Hardman C S, Camelo A, Bucks C, Wu X, Kane C M, Neill D R, Flynn R J, Sayers I, Hall I P and McKenzie N J. (2013). IL-33 is more potent than IL-25 in provoking IL-13–producing nuocytes (type 2 innate lymphoid cells) and airway contraction. American Academy of Allergy, Asthma & Immunology,
  • Barnes P. (2001).Th2 cytokines and asthma: an introduction. Respir Res., 2, 64–65.
  • Bhakta N R and Woodruff P G. (2011). Human asthma phenotypes: from the clinic, to cytokines, and back again. Immunol. Rev,242, 220–32.
  • Cayrol C and Girard J P. (2014). IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy. Curr Opin Immunol, 31,31-7.
  • Cayrol C, Duval A, Schmitt P, Roga S, Camus M, Stella A, Burlet-Schiltz O, Gonzalez-de-Peredo A. and Girard J-P. (2018). Environmental allergens induce allergic inflammation through proteolytic maturation of IL-33. Nat Immunol, 140,777.
  • Cheung P F, Wong C K, Ip W K and Lam C W. (2006). IL- 25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. Allergy, 61, 878–885.
  • Coban H and Ediger D (2018) Control of asthma, quality of life, anxiety and depression symptoms among Turkish patients with asthma. Electronic Journal of General Medicine, 15(5), em71.
  • Dold S, Wjst M, von Mutius E, Reitmeir P and Stiepel E. (1992). Genetic risk for asthma, allergic rhinitis, and atopic dermatitis. Archives of Disease in Childhood, 67, 1018-1022.
  • Elliott L, Jr Samuel J A, Harvey E S, Lee R C, Salo P M, Cohn R D, London S J and Zeldin D C. (2007). Dust Weight and Asthma Prevalence in the National Survey of Lead and Allergens in Housing (NSLAH). Environ Health Perspect, 115(2),215–220.
  • Fulgheri G and Malinowski B. (2011). The role of IL-33 in the inflammation process of asthma and atherosclerosis. eJIFCC, 22 (3), 079-091.
  • Hansel T T, Johnston S L and Openshaw P J. (2013). Microbes and mucosal immune responses in asthma. Lancet. Mar 9, 381(9869), 861–873.
  • Hassanpour K, Tehrani H, Goudarzian M, Beihaghi S, Ebrahimi M and Amiri P (2019) Comparison of the frequency of dental caries in asthmatic children under treatment with inhaled corticosteroids and healthy children in Sabzevar in 2017-2018. Electronic Journal of General Medicine, 16(2), em119.
  • Holgate S T. (2012). Innate and adaptive immune responses in asthma. Nat.Med, 18, 673–83.
  • Hubaida F and Dawn C. (2017). Newcomb. Mechanisms driving gender differences in asthma. Curr Allergy Asthma Rep., 17(3), 19.
  • Kearley J, Silver J S, Sanden C, Liu Z, Berlin A A, White N, Mori M, Pham T, Ward C K, Criner J, Marchetti N, Mustelin T, Erjefalt J S, Kolbeck R and Humbles A. A. (2015). Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection. Immunity, 42, 566-79.
  • Kouzaki H, Tojima I, Kita H. and Shimizu T. (2013). Transcription of interleukin-25 and extracellular release of the protein is regulated by allergen proteases in airway epithelial cells. Am J Respir Cell Mol Biol., 49,741-50.
  • Kynyk J A, Mastronarde J G and McCallister J W. (2011). Asthma, the sex difference. Curr Opin Pulm Med., 17(1), 6–11.
  • Leuthi A U, Cullen S P, McNeela E A, Duriez P J, Afonina I S, Sheridan C. Brumatti G, Taylor R C, Kersse K, Vandenabeele P, Lavelle E C and Martin S J. (2009). Suppression of interleukin-33 bioactivity through proteolysis by apoptotic caspases. Immunity, 31,84-98.
  • Liu Y, Shao Z, Shangguan G, Bie Q and Zhang B (2018). Biological Properties and the Role of IL-25 in Disease Pathogenesis. Journal of Immunology Research, Article ID 6519465, 8 pages.
  • Martin N T and Martin M U. (2016). Interleukin 33 is a guardian of barriers and a local alarmin. Nat Immunol, 17,122-31.
  • Molofsky A B, Savage A K and Locksley R M. (2015). Interleukin-33 in tissue homeostasis, injury, and inflammation. Immunity, 42,1005-19.
  • Momen T, Ahanchian H, Reisi M, Shamsdin S A, Shahsanai A and Keivanfar M (2017). Comparison of Interleukin-33 Serum Levels in Asthmatic Patients with a Control Group and Relation with the Severity of the Disease. Int J Prev Med, 8, 65.
  • Murdoch J E and Lloyd C M. (2010). Chromic inflammation and asthma. Mutat Res., 690 (1-2), 24–39.
  • Paplińska -Goryca M, Grabczak E M, Dąbrowska M, Hermanowicz-Salamon J, Proboszcz M, Nejman-Gryz P, Maskey-Warzęchowska M and Krenke R. (2018). Sputum interleukin-25 correlates with asthma severity: a preliminary study. Advances in Dermatology and Allergology,35 (5), 462–469.
  • Polosa R and Thomson N C. (2013). Smoking and asthma: dangerous liaisons European Respiratory Journal., 41, 716-726.
  • Préfontaine D, Lajoie-Kadoch S, Foley S, Audusseau S, Olivenstein R, Halayko A J, Lemière C, Martin J G and Hamid Q. (2009). Increased expression of IL-33 in severe asthma: Evidence of expression by airway smooth muscle cells. J Immunol.,183, 5094–103.
  • Préfontaine D, Nadigel J, Chouiali F, Audusseau S, Semlali A, Chakir J, Martin J G and Hamid Q (2010). Increased IL-33 expression by epithelial cells in bronchial asthma. J Allergy Clin Immunol.,125,752–4.
  • Sharkhuu T, Matthaei K I, Forbes E, Mahalingam S., Hogan S. P., Hansbro P. M. and Foster P. S. (2006). Mechanism of interleukin-25 (IL-17E)-induced pulmonary inflammation and airways hyper-reactivity. Clin Exp Allergy, 36, 1575-83.
  • Steiner U C, Bachmann L M, Soyka M B, Regenass S, Steinegger L and Probst E. (2018). Relationship Between Rhinitis, Asthma, and Eczema and the Presence of Sensitization in Young Swiss Adults. Allergy & Rhinology, 9, 1–6.
  • Steven A. S, Mark C. S, Jacqueline G. P, Sean P. S., Joseph F. U. Jr., Joel E. T., Alison L. B., Melanie A. K., Robert A. K., Taku K., Avinash B., and David A. (2010). IL25 elicits a multipotent progenitor cell population that promotes T(H)2 cytokine responses. Nature, 464, 1362–1366.
  • Tamachi T, Maezawa Y, Ikeda K, Kagami S, Hatano M, Seto Y, Suto A, Suzuki K, Watanabe N, Saito Y, Tokuhisa T, Iwamoto I, and Nakajima H. (2006). IL-25 enhances allergic airway inflammation by amplifying a Th2 cell-dependent pathway in mice. J Allergy Clin Immunol, 118, 606-14.
  • Terrier B, Bièche I, Maisonobe T, Laurendeau I, Rosenzwajg M, Kahn J E,Diemert M C, Musset L, Vidaud M, Sène D, Costedoat-Chalumeau N, Thi- Huong D L, Amoura Z, Klatzmann D, Cacoub P and David Saadoun. (2010). Interleukin-25: a cytokine linking eosinophils and adaptive immunity in Churg-Strauss syndrome. Blood, 116, 4523-31.
  • Trinh P, Jung T H, Keene D, Demmer R T, Perzanowski M and Lovasi G. (2018). Temporal and spatial associations between influenza and asthma hospitalisations in New York City from 2002 to 2012: a longitudinal ecological study. BMJ Open, 8, e020362.
  • Tworek D, Majewski S, Szewczyk K, Kiszałkiewicz J, Kurmanowska Z, Górski P, Brzeziańska-Lasota E, Kuna P and Antczak A. (2018). The association between airway eosinophilic inflammation and IL-33 in stable non-atopic COPD. Respiratory Research, 19,108.
  • Wang C, Liu Q, Chen F, Xu W, Zhang C and Xiao W. (2016). IL-25 Promotes Th2 Immunity Responses in Asthmatic Mice via Nuocytes Activation. PLOS ONE, September 12. DOI:10.1371/journal.pone.0162393.
  • Wong C K, Cheung P F, Ip W K and Lam C W. (2005). Interleukin- 25-induced chemokines and interleukin-6 release from eosinophils is mediated by p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, and nuclear factorkappaB. Am J Respir Cell Mol Biol., 33, 186–194.


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