The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines
Background. Airway epithelium plays an important role during the development of allergic rhinitis (AR), which is characterized by production of thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25). IL-35, mainly expressed by Treg cells, have negative regulation in...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2021/1110671 |
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| _version_ | 1832565677449281536 |
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| author | Mingrong Nie Qingxiang Zeng Luo Xi Yiquan Tang Renzhong Luo Wenlong Liu |
| author_facet | Mingrong Nie Qingxiang Zeng Luo Xi Yiquan Tang Renzhong Luo Wenlong Liu |
| author_sort | Mingrong Nie |
| collection | DOAJ |
| description | Background. Airway epithelium plays an important role during the development of allergic rhinitis (AR), which is characterized by production of thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25). IL-35, mainly expressed by Treg cells, have negative regulation in Th2, Th17, and ILC2 inflammation. However, the effect of IL-35 on human nasal epithelial cells (HNECs) especially the secretion of nasal epithelial-derived proinflammatory cytokines as well as the possible mechanism is still unclear. Methods. HNECs were cultured and stimulated by various stimulators. The expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 from supernatant was measured using real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). AR mice were developed to verify the effect of IL-35 on nasal epithelial cells in vivo. Results. After Poly I:C stimulation, IL-35 inhibited the production of IL-25, and TSLP from HNECs increased significantly compared with baseline levels (P<0.05). After Dermatophagoides pteronyssinus or Aspergillus fumigatus stimulation, IL-35 inhibited the production of IL-25, IL-33, and TSLP from HNECs increased significantly compared with baseline levels (P<0.05). After Dermatophagoides pteronyssinus, IL-35 inhibited the production of eotaxin-1, eotaxin-2, and eotaxin-3 released from HNECs increased significantly compared with baseline levels (P<0.05). Similarly, IL-35-treated AR mice presented with decreased expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 in nasal lavage fluid. Conclusion. IL-35 suppressed both type 2 inflammation-inducing cytokines and eosinophil chemotactic factor from HNECs, suggesting the important role of IL-35 during the development of AR. |
| format | Article |
| id | doaj-art-d1e54b75bfff4378a2e724007cc5b753 |
| institution | Kabale University |
| issn | 1466-1861 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-d1e54b75bfff4378a2e724007cc5b7532025-02-03T01:07:07ZengWileyMediators of Inflammation1466-18612021-01-01202110.1155/2021/1110671The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory CytokinesMingrong Nie0Qingxiang Zeng1Luo Xi2Yiquan Tang3Renzhong Luo4Wenlong Liu5Department of OtolaryngologyDepartment of OtolaryngologyDepartment of OtolaryngologyDepartment of OtolaryngologyDepartment of OtolaryngologyDepartment of OtolaryngologyBackground. Airway epithelium plays an important role during the development of allergic rhinitis (AR), which is characterized by production of thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25). IL-35, mainly expressed by Treg cells, have negative regulation in Th2, Th17, and ILC2 inflammation. However, the effect of IL-35 on human nasal epithelial cells (HNECs) especially the secretion of nasal epithelial-derived proinflammatory cytokines as well as the possible mechanism is still unclear. Methods. HNECs were cultured and stimulated by various stimulators. The expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 from supernatant was measured using real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). AR mice were developed to verify the effect of IL-35 on nasal epithelial cells in vivo. Results. After Poly I:C stimulation, IL-35 inhibited the production of IL-25, and TSLP from HNECs increased significantly compared with baseline levels (P<0.05). After Dermatophagoides pteronyssinus or Aspergillus fumigatus stimulation, IL-35 inhibited the production of IL-25, IL-33, and TSLP from HNECs increased significantly compared with baseline levels (P<0.05). After Dermatophagoides pteronyssinus, IL-35 inhibited the production of eotaxin-1, eotaxin-2, and eotaxin-3 released from HNECs increased significantly compared with baseline levels (P<0.05). Similarly, IL-35-treated AR mice presented with decreased expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 in nasal lavage fluid. Conclusion. IL-35 suppressed both type 2 inflammation-inducing cytokines and eosinophil chemotactic factor from HNECs, suggesting the important role of IL-35 during the development of AR.http://dx.doi.org/10.1155/2021/1110671 |
| spellingShingle | Mingrong Nie Qingxiang Zeng Luo Xi Yiquan Tang Renzhong Luo Wenlong Liu The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines Mediators of Inflammation |
| title | The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines |
| title_full | The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines |
| title_fullStr | The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines |
| title_full_unstemmed | The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines |
| title_short | The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines |
| title_sort | effect of il 35 on the expression of nasal epithelial derived proinflammatory cytokines |
| url | http://dx.doi.org/10.1155/2021/1110671 |
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