![]() ![]() Kauffman HF (2003) Interaction of environmental allergens with airway epithelium as a key component of asthma. J Immunol 169:5904–5911īalenga NA, Klichinsky M, Xie Z, Chan EC, Zhao M, Jude J, Laviolette M, Panettieri RA Jr, Druey KM (2015) A fungal protease allergen provokes airway hyper-responsiveness in asthma. Kheradmand F, Kiss A, Xu J, Lee SH, Kolattukudy PE, Corry DB (2002) A protease-activated pathway underlying Th cell type 2 activation and allergic lung disease. Proc Natl Acad Sci USA 94:1344–1349Ĭorry DB, Grunig G, Hadeiba H, Kurup VP, Warnock ML, Sheppard D, Rennick DM, Locksley RM (1998) Requirements for allergen-induced airway hyperreactivity in T and B cell-deficient mice. Mehlhop PD, van de Rijn M, Goldberg AB, Brewer JP, Kurup VP, Martin TR, Oettgen HC (1997) Allergen-induced bronchial hyperreactivity and eosinophilic inflammation occur in the absence of IgE in a mouse model of asthma. Lindsay R, Slaughter T, Britton-Webb J, Mog SR, Conran R, Tadros M, Earl N, Fox D, Roberts J, Bolger WE (2006) Development of a murine model of chronic rhinosinusitis. Lee KI, Kim DW, Kim EH, Kim JH, Samivel R, Kwon JE, Ahn JC, Chung YJ, Mo JH (2014) Cigarette smoke promotes eosinophilic inflammation, airway remodeling, and nasal polyps in a murine polyp model. Shin HW, Kim DK, Park MH, Eun KM, Lee M, So D, Kong IG, Mo JH, Yang MS, Jin HR, Park JW, Kim DW (2015) IL-25 as a novel therapeutic target in nasal polyps of patients with chronic rhinosinusitis. Histopathol Allergy Asthma Proc 17:237–242 Kim SW, Kim JH, Jung MH, Hur DG, Lee HK, Jeon SY, Kim DW (2013) Periostin may play a protective role in the development of eosinophilic chronic rhinosinusitis with nasal polyps in a mouse model. Kim DW, Khalmuratova R, Hur DG, Jeon SY, Kim SW, Shin HW, Lee CH, Rhee CS (2011) Staphylococcus aureus enterotoxin B contributes to induction of nasal polypoid lesions in an allergic rhinosinusitis murine model. Kim JH, Yi JS, Gong CH, Jang YJ (2014) Development of Aspergillus protease with ovalbumin-induced allergic chronic rhinosinusitis model in the mouse. Payne SC, Borish L, Steinke JW (2011) Genetics and phenotyping in chronic sinusitis. Zhang N, Van Zele T, Perez-Novo C, Van Bruaene N, Holtappels G, DeRuyck N, Van Cauwenberge P, Bachert C (2008) Different types of T-effector cells orchestrate mucosal inflammation in chronic sinus disease. McGarry G, Melia L (2009) Nasal polyps: an update. In conclusion, intranasal AP and OVA exposure successfully induced Th2-specific CRSwNP in a murine model.Ĭhaaban MR, Walsh EM, Woodworth BA (2013) Epidemiology and differential diagnosis of nasal polyps. In contrast, eotaxin levels were particularly elevated in the sinonasal mucosa and nasal lavage fluid in the 12-week group. INF-γ and IL-17A were undetectable or not elevated relative to the control group levels. The IL-4, IL-5, and IL-13 mRNA and protein levels were elevated in the sinonasal mucosa and nasal lavage fluid. Polypoid mucosal lesions were predominantly observed in the 12-week group, which also exhibited mucosal thickening on micro-CT scans. Greater eosinophil infiltration in the subepithelial layer was observed in the challenged groups, compared with the control group. Protein levels of Th2 cytokines, INF-γ, IL-17A, and chemokines in nasal lavage fluid, and total serum IgE were measured by ELISA. Sinonasal samples were evaluated histologically, and interleukin (IL)-4, IL-5, IL-13, eotaxin, keratinocyte chemoattractant, and macrophage inflammatory protein-2 mRNA levels in sinonasal mucosa were measured by real-time PCR. C57BL/6 mice were challenged intranasally with a mixture of an Aspergillus oryzae-derived protease (AP) and ovalbumin (OVA) for 6, 8, or 12 consecutive weeks (12 mice/group) control mice received the same volume of phosphate-buffered saline for 12 weeks ( n = 12). Here, we aimed to establish an eosinophilic CRSwNP murine model, which would be essential to understand the underlying pathogenesis and establish a treatment strategy. One subtype of chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by the development of a T-helper type 2 (Th2) response and eosinophilic infiltration. ![]()
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