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Interleukin-25 Enhances Allergic Inflammation through p38MAPK and NF-κB Pathways in Mouse Models of Allergic Rhinitis

Abstract

Interleukin (IL)-25, a cytokine of IL-17 family, can activate p38 Mitogen-Activated Protein kinases(MAPK) and Nuclear Factor(NF)-κB pathways to propagate Th2 responses. The allergic rhinitis mouse model was established by stimulating BALB/c mouse with ovalbumin (OVA). Then we detected expression of IL-25 and downstream p38MAPK and NF-κB. The expression of IL-25, p38MAPK and NF-κB were detected in the OVA-induced allergic rhinitis mouse model. The allergic parameters, such as allergic symptoms, serum OVA-specific immunoglobulin E (IgE) levels and eosinophil infiltration in the nasal mucosa were compared between OVA group and control group. OVA-induced mice displayed significantly higher allergic responses compared with the saline control group. OVA induced mice demonstrated more allergic symptoms, higher serum OVA-specific IgE levels and eosinophil infiltrations. The increased expression of IL-25, p38MAPK and NF-κB immunoreactivity were detected in epidermal cells in the OVA group. The mRNA measurement of IL-25, p38MAPK and NF-κB showed the same result. IL-25 enhances the OVA-induced allergic rhinitis by activating p38MAPK and NF-κB pathways.

1. Brozek JL, Bousquet J, Baena-Cagnani CE, Bonini S, Canonica GW, Casale TB, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines: 2010 revision. J Allergy Clin Immunol 2010; 126(3):466-476.
2. Maurer M, Zuberbier T. Under treatment of rhinitis symptoms in Europe: findings from a cross-sectional questionnaire survey. Allergy 2007; 62(9):1057–63.
3. Uzzaman A, Story R. Chapter 5: Allergic rhinitis. Allergy Asthma Proc 2012; 33(Suppl 1):S15-8.
4. Bousquet J, Khaltaev N, Cruz AA, Denburg J, Fokkens WJ, Togias A, et al. Allergic Rhinitis and its Impact on Asthma (ARIA) 2008. Allergy 2008; 63(Suppl 86):8-160.
5. Barnes PJ. Pathophysiology of allergic inflammation.Immunol Rev 2011; 242(1):31–50.
6. Saadoun D, Terrier B, Cacoub P. Interleukin-25: Key Regulator of Inflammatory and Autoimmune Diseases. Curr Pharm Des 2011; 17(34):3781-5.
7. Sharkhuu T, Matthaei KI, Forbes E, Mahalingam S,Hogan SP, Hansbro PM, et al. Mechanism of interleukin-25(IL-17E)-induced pulmonary inflammation and airways hyper-reactivity. Clin Exp Allergy 2006;36(12):1575-83.
8. Petersen BC, Budelsky AL, Baptist AP, Schaller MA, Lukacs NW. Interleukin-25 induces type 2 cytokine production in a steroid-resistant interleukin-17RB+ myeloid population that exacerbates asthmatic pathology. Nat Med 2012; 18(5):751-8.
9. Tamachi T, Maezawa Y, Ikeda K, Iwamoto I, Nakajima H. Interleukin 25 in allergic airway inflammation. Int Arch Allergy Immunol 2006; 140(Suppl 1):59-62.
10. Wong CK, Cheung PFY, Ip WK, Lam CWK. 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 Factor-κB. Am J Respir Cell Mol Biol 2005; 33(2):186-94.
11. Liu J, Liu L, Cui Y, Zhang J, Jiang H. p38 MAPK regulates Th2 cytokines release in PBMCs in allergic rhinitis rats. J Huazhong Univ Sci Technolog Med Sci 2010; 30(2):222-5.
12. Hu H, Wu X, Jin W, Chang M, Cheng X, Sun SC.Noncanonical NF-kappaB regulates inducible costimulator (ICOS) ligand expression and T follicular helper cell development. Proc Natl Acad Sci U S A 2011;108(31):12827-32.
13. Bartemes KR, Kita H. Dynamic role of epithelium- derived cytokines in asthma. Clin Immunol 2012;143(3):222-35.
14. Sun SC. Non-canonical NF-kappaB signaling pathway. Cell Res 2011; 21(1):71-85.
15. Zheng C, Yin Q, Wu H. Structural studies of NF-kappaB signaling. Cell Res 2011; 21(1):183-95.
16. Wong CK, Li PW, Lam CW. Intracellular JNK, p38 MAPK and NF-kappaB regulate IL-25 induced release of cytokines and chemokines from costimulated T helper lymphocytes. Immunol Lett 2007; 112(2):82-91.
17. Ozdoganoglu T, Songu M. The burden of allergic rhinitis and asthma. Ther Adv Respir Dis 2012; 6(1):11-23.
18. Tamachi T, Maezawa Y, Ikeda K, Kagami S, Hatano M, Seto Y et al. IL-25 enhances allergic airway inflammation by amplifying a TH2 cell-dependent pathway in mice. J Allergy Clin Immunol 2006; 118(3):606-14.
19. Swaidani S, Bulek K, Kang Z, Caini Liu, Weiguo Yin,Amina Abbadi et al. T Cell-Derived Act1 Is Necessary for IL-25-Mediated Th2 Responses and Allergic Airway Inflammation. J Immunol 2011; 187(6):3155-64.
20. Cheung PF, Wong CK, Ip WK, Lam CW. IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation. Allergy 2006; 61:878-85.
21. Dong C. Regulation and pro-inflammatory function of interleukin-17 family cytokines. Immunol Rev 2008;226:80-6.
22. Ballantyne SJ, Barlow JL, Jolin HE, Nath P, Williams AS, Chung KF, et al. Blocking IL-25 prevents airway hyperresponsiveness in allergic asthma. J Allergy Clin Immunol 2007; 120(6):1324-31.
23. Corrigan CJ, Wang W, Meng Q, Fang C, Wu H, Reay V, et al. T-helper cell type 2 (Th2) memory T cell-potentiating cytokine IL-25 has the potential to promote angiogenesis in asthma. Proc Natl Acad Sci U S A 2011;108(4):1579-84.
24. Hurst SD, Muchamuel T, Gorman DM, Gilbert JM, Clifford T, Kwan S, et al. New IL-17 Family Members Promote Th1 or Th2 Responses in the Lung: In Vivo Function of the Novel Cytokine IL-25. J Immunol 2002;169(1):443-53.
25. Hayden MS, Ghosh S. NF-kappaB in immunobiology.Cell Res 2011; 21(2):223-44.
26. Lesueur C, Bôle-Feysot C,, Bekri S, Husson A, Lavoinne A, Brasse-Lagnel C. Glutamine induces nuclear degradation of the NF-κB p65 subunit in Caco-2/TC7 cells. Biochimie 2012; 94(3):806-15.

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IssueVol 13, No 6 (2014) QRcode
SectionArticles
Keywords
Allergic rhinitis Interleukin-25 Mice NF-kappa B p38 Mitogen-Activated

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How to Cite
1.
Li Z, Wang H, Liu L. Interleukin-25 Enhances Allergic Inflammation through p38MAPK and NF-κB Pathways in Mouse Models of Allergic Rhinitis. Iran J Allergy Asthma Immunol. 1;13(6):412-419.