Sung-Lyong Hong1,2,3, Yu-Lian Zhang4, Sang-Wook Kim5, Dae Woo Kim4,6, Sang-Heon Cho3,7, Yoon-Seok Chang8, Chul Hee Lee4,9, Chae-Seo Rhee3,9,10,11. 1. Department of Otorhinolaryngology-Head and Neck Surgery, Pusan National University Hospital, Busan, South Korea. 2. Medical Research Institute, Pusan National University Hospital, Busan, South Korea. 3. Graduate School of Immunology, Seoul National University College of Medicine, Seoul, South Korea. 4. Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, South Korea. 5. Department of Otorhinolaryngology, Gyeongsang National University, Jinju, South Korea. 6. Department of Otorhinolaryngology, Seoul National University Boramae Medical Center, Seoul, South Korea. 7. Department of Internal Medicine, Seoul National University Hospital, Seoul, South Korea. 8. Department of Internal Medicine, Seoul National University Bundang Hospital, Gyeonggi, South Korea. 9. Department of Otorhinolaryngology, Seoul National University Bundang Hospital, Gyeonggi, South Korea. 10. Research Center for Sensory Organs, Seoul National University Medical Research Center, Seoul, South Korea. 11. Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea.
Abstract
BACKGROUND: Nasal polyposis associated with chronic rhinosinusitis (CRS) is a chronic inflammatory disease that is characterized by infiltration of many inflammatory cells. Meanwhile, interleukin (IL)-17A is a well-known proinflammatory cytokine that induces both eosinophilic and neutrophilic inflammation. We investigated the role of IL-17A in the development of nasal polyps in the CRS murine model. METHODS: Eosinophilic CRS with nasal polyps was induced by using ovalbumin (OVA) and Staphylococcus aureus enterotoxin B (SEB) in wild-type BALB/c and IL-17A knockout (KO) mice. Histopathologic changes of the sinonasal cavity were evaluated using hematoxylin and eosin, Periodic acid-Schiff, Sirius red, Masson's trichrome, and immunohistochemistry. The levels of total and OVA-specific immunoglobulin Es (IgEs) in sera were measured using enzyme-linked immunosorbent assay. The expression levels of IL-4, IL-5, and interferon-γ (IFN-γ) in the nasal mucosa were assessed by quantitative real-time polymerase chain reaction. RESULTS: Under the IL-17A deficiency, total and OVA-specific IgEs in sera were reduced significantly. Infiltration of both eosinophils and neutrophils into the nasal mucosa, subepithelial fibrosis, and goblet cell count also decreased significantly in IL-17A KO mice treated with both OVA and SEB compared with those in the wild-type counterpart. However, there were no significant differences in the number of polypoid lesions among groups. Meanwhile, IL-4 increased and IFN-γ decreased in the nasal mucosa in IL-17A KO mice treated with both OVA and SEB. CONCLUSION: This study suggests that even though IL-17A plays an important role in both nasal inflammation and remodeling, it does not influence the development of nasal polypoid lesions.
BACKGROUND: Nasal polyposis associated with chronic rhinosinusitis (CRS) is a chronic inflammatory disease that is characterized by infiltration of many inflammatory cells. Meanwhile, interleukin (IL)-17A is a well-known proinflammatory cytokine that induces both eosinophilic and neutrophilic inflammation. We investigated the role of IL-17A in the development of nasal polyps in the CRS murine model. METHODS:Eosinophilic CRS with nasal polyps was induced by using ovalbumin (OVA) and Staphylococcus aureus enterotoxin B (SEB) in wild-type BALB/c and IL-17A knockout (KO) mice. Histopathologic changes of the sinonasal cavity were evaluated using hematoxylin and eosin, Periodic acid-Schiff, Sirius red, Masson's trichrome, and immunohistochemistry. The levels of total and OVA-specific immunoglobulin Es (IgEs) in sera were measured using enzyme-linked immunosorbent assay. The expression levels of IL-4, IL-5, and interferon-γ (IFN-γ) in the nasal mucosa were assessed by quantitative real-time polymerase chain reaction. RESULTS: Under the IL-17A deficiency, total and OVA-specific IgEs in sera were reduced significantly. Infiltration of both eosinophils and neutrophils into the nasal mucosa, subepithelial fibrosis, and goblet cell count also decreased significantly in IL-17A KO mice treated with both OVA and SEB compared with those in the wild-type counterpart. However, there were no significant differences in the number of polypoid lesions among groups. Meanwhile, IL-4 increased and IFN-γ decreased in the nasal mucosa in IL-17A KO mice treated with both OVA and SEB. CONCLUSION: This study suggests that even though IL-17A plays an important role in both nasal inflammation and remodeling, it does not influence the development of nasal polypoid lesions.
Authors: Anuj Tharakan; Alex Dobzanski; Nyall R London; Syed M Khalil; Nitya Surya; Andrew P Lane; Murugappan Ramanathan Journal: Int Forum Allergy Rhinol Date: 2018-01-17 Impact factor: 3.858
Authors: Gwanghui Ryu; Jun Sang Bae; Ji Hye Kim; Eun Hee Kim; Lele Lyu; Young Jun Chung; Ji Hun Mo Journal: Allergy Asthma Immunol Res Date: 2020-05 Impact factor: 5.764