The Roles of Interleukin-17A/F and IL-36Ra in Obese Asthmatic Children

Yıl 2022, Cilt: 4 Sayı: 1, 10 - 17, 30.04.2022

Aziza Buabraig , Resul Karakuş

Öz

Childhood asthma and obesity are serious and chronic public health problems that require specific treatment. The prevalence of asthma in obese individuals is higher than that of non-obese individuals. Despite the belief that obesity is a major risk factor in the development of asthma, the mechanisms and effects associated with obesity are yet to be explained. It was considered that these two diseases are associated with excess adipose tissue that predisposes patients to inflammation and could contribute to the pathogenesis and severity of asthma. IL-17A and IL-17F are cytokines with pro-inflammatory properties, and high levels were observed in the serum of children with asthma and obesity. Also, IL-36 is a proinflammatory cytokine that acts as a mediator between the innate and adaptive immune systems to induce CXCL8 and IL-17 expressions. It could be suggested that these pro-inflammatory cytokines could play a role in the association between the two conditions. However, the activities of these cytokines are inhibited by anti-inflammatory cytokines such as IL-36Ra. The present review aims to explain the role of proinflammatory cytokines in adipose tissue and airway structure, as well as the association between the Th17 cytokines and the IL-36 cytokine family.

Anahtar Kelimeler

Obesity, Asthma, IL-17A, IL-17F, IL-36, IL-36Ra

Kaynakça

• 1. Okubo, Y., et al. (2017) Impact of pediatric obesity on acute asthma exacerbation in Japan. Pediatric Allergy and Immunology, 28(8): p. 763-767.
• 2. Lang, J.E., et al. (2018) Being overweight or obese and the development of asthma. Pediatrics, 142(6).
• 3. Di Genova, L., et al. (2018) Children with obesity and asthma: which are the best options for their management? Nutrients, 10(11): p. 1634.
• 4. Youssef, D.M., et al. (2013)The influence of leptin on Th1/Th2 balance in obese children with asthma. Jornal Brasileiro de Pneumologia, 39: p. 562-568.
• 5. Leija-Martínez, J.J., et al. (2020) Decreased methylation profiles in the TNFA gene promoters in type 1 macrophages and in the IL17A and RORC gene promoters in Th17 lymphocytes have a causal association with non-atopic asthma caused by obesity: a hypothesis. Medical hypotheses, 134: p. 109527.
• 6. O'Sullivan, B.P., et al. (2021) Obesity‐related asthma in children: A role for vitamin D. Pediatric pulmonology, 56(2): p. 354-361.
• 7. Rastogi, D. (2020)Pediatric obesity‐related asthma: A prototype of pediatric severe non‐T2 asthma. Pediatric pulmonology, 55(3): p. 809-817.
• 8. Reilly, J.J. (2005) Descriptive epidemiology and health consequences of childhood obesity. Best practice & research Clinical endocrinology & metabolism, 19(3): p. 327-341.
• 9. Peters, U., A.E. Dixon, and E. Forno. (2018) Obesity and asthma. Journal of Allergy and Clinical immunology, 141(4): p. 1169-1179.
• 10. Lumeng, C.N., J.L. Bodzin, and A.R. Saltiel. (2007) Obesity induces a phenotypic switch in adipose tissue macrophage polarization. The Journal of clinical investigation, 117(1): p. 175-184.
• 11. Chehimi, M., H. Vidal, and A. Eljaafari. (2017) Pathogenic role of IL-17-producing immune cells in obesity, and related inflammatory diseases. Journal of clinical medicine, 6(7): p. 68.
• 12. Mraz, M. and M. Haluzik. (2014) The role of adipose tissue immune cells in obesity and low-grade inflammation. Journal of Endocrinology, 222(3): p. R113-R127.
• 13. Hayran, Y., et al. (2020) Serum IL-36α, IL-36β, and IL-36γ levels in patients with hidradenitis suppurativa: Association with disease characteristics, smoking, obesity, and metabolic syndrome. Archives of dermatological research, 312(3): p. 187-196.
• 14. Moermans, C., et al.(2021)Sputum IL-25, IL-33 and TSLP, IL-23 and IL-36 in airway obstructive diseases. Reduced levels of IL-36 in eosinophilic phenotype. Cytokine, 140: p. 155421.
• 15. Kudo, M., et al.(2012) IL-17A produced by αβ T cells drives airway hyper-responsiveness in mice and enhances mouse and human airway smooth muscle contraction. Nature medicine, 18(4): p. 547-554.
• 16. Stockinger, B. and M. Veldhoen, (2007)Differentiation and function of Th17 T cells. Current opinion in immunology, 19(3): p. 281-286.
• 17. Newcomb, D.C. and R.S. Peebles Jr. (2013)Th17-mediated inflammation in asthma. Current opinion in immunology, 25(6): p. 755-760.
• 18. Bettelli, E., et al.(2008) Induction and effector functions of TH 17 cells. Nature, 453(7198): p. 1051-1057.
• 19. Eyerich, K., V. Dimartino, and A. Cavani. (2017) IL‐17 and IL‐22 in immunity: Driving protection and pathology. European journal of immunology, 47(4): p. 607-614.
• 20. Ricciardolo, F.L., et al. (2017)Identification of IL-17F/frequent exacerbator endotype in asthma. Journal of Allergy and Clinical Immunology, 140(2): p. 395-406.
• 21. Carrier, Y., et al.(2011)Inter-regulation of Th17 cytokines and the IL-36 cytokines in vitro and in vivo: implications in psoriasis pathogenesis. Journal of Investigative Dermatology, 131(12): p. 2428-2437.
• 22. Vigne, S., et al.(2011) IL-36R ligands are potent regulators of dendritic and T cells. Blood, The Journal of the American Society of Hematology, 118(22): p. 5813-5823.
• 23. Bridgewood, C., et al. (2017) IL‐36γ has proinflammatory effects on human endothelial cells. Experimental dermatology, 26(5): p. 402-408.
• 24. Queen, D., C. Ediriweera, and L. Liu. (2019) Function and regulation of IL-36 signaling in inflammatory diseases and cancer development. Frontiers in cell and developmental biology, 7: p. 317.
• 25. Sun, K., C.M. Kusminski, and P.E. Scherer. (2011) Adipose tissue remodeling and obesity. The Journal of clinical investigation,121(6): p. 2094-2101.
• 26. Al Heialy, S., et al. (2020) Contribution of IL-17 in steroid hyporesponsiveness in obese asthmatics through dysregulation of glucocorticoid receptors α and β. Frontiers in Immunology, 11: p. 1724.
• 27. Schindler, T.I., et al. (2017) TH17 cell frequency in peripheral blood is elevated in overweight children without chronic inflammatory diseases. Frontiers in immunology, 8: p. 1543.
• 28. Łuczyński, W., et al. (2015) Elevated levels of Th17 cells in children with central obesity. Scandinavian journal of clinical and laboratory investigation, 75(7): p. 595-601.
• 29. Lindén, A. (2006) Interleukin-17 and airway remodelling. Pulmonarypharmacology & therapeutics, 19(1): p. 47-50.
• 30. Lindén, A. (2001) Role of interleukin-17 and the neutrophil in asthma. International archives of allergy and immunology,126(3): p. 179-184.
• 31. Hoshino, H., et al. (2000) Increased elastase and myeloperoxidase activity associated with neutrophil recruitment by IL-17 in airways in vivo. Journal of Allergy and Clinical Immunology, 105(1): p. 143-149.
• 32. Chen, Y., et al. (2003) Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Journal of Biological Chemistry, 278(19): p. 17036-17043.
• 33. Mathews, J.A., et al. (2014) Induction of IL-17A precedes development of airway hyperresponsiveness during diet-induced obesity and correlates with complement factor D. Frontiers in immunology, 5: p. 440.
• 34. Han, Y.-Y., et al. (2015) Diet, interleukin-17, and childhood asthma in Puerto Ricans. Annals of Allergy, Asthma & Immunology,115(4): p. 288-293. e1.
• 35. Giannoudaki, E., et al. (2019) Interleukin-36 cytokines alter the intestinal microbiome and can protect against obesity and metabolic dysfunction. Nature communications, 10(1): p. 1-14.
• 36. Van Asseldonk, E.J., et al. (2010) The effect of the interleukin‐1 cytokine family members IL‐1F6 and IL‐1F8 on adipocyte differentiation. Obesity, 18(11): p. 2234-2236.
• 37. Ramadas, R.A., et al. (2011) Interleukin-1 family member 9 stimulates chemokine production and neutrophil influx in mouse lungs. American journal of respiratory cell and molecular biology, 44(2): p. 134-145.
• 38. Liu, X.-G., et al.(2020). Interleukin-36 receptor antagonist alleviates airway inflammation in asthma via inhibiting the activation of interleukin-36 pathway. International immunopharmacology, 81: p. 106200.