Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin
Abstract Exposure to various antigens derived from house dust mites (HDM) is considered to be a risk factor for development of certain allergic diseases such as atopic asthma, atopic dermatitis, rhinitis and conjunctivitis. Chitin is an insoluble polysaccharide (β-(1–4)-poly-N-acetyl-d-glucosamine)...
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2021
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oai:doaj.org-article:b2ff8b41fa784b708de791905ef9f7432021-12-02T11:39:33ZInterleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin10.1038/s41598-021-85277-42045-2322https://doaj.org/article/b2ff8b41fa784b708de791905ef9f7432021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85277-4https://doaj.org/toc/2045-2322Abstract Exposure to various antigens derived from house dust mites (HDM) is considered to be a risk factor for development of certain allergic diseases such as atopic asthma, atopic dermatitis, rhinitis and conjunctivitis. Chitin is an insoluble polysaccharide (β-(1–4)-poly-N-acetyl-d-glucosamine) and a major component in the outer shell of HDMs. Mice exposed to chitin develop asthma-like airway eosinophilia. On the other hand, several lines of evidence show that the effects of chitin on immune responses are highly dependent on the size of chitin particles. In the present study, we show that chitin induced production of IL-33 and TSLP by alveolar and bronchial epithelial cells, respectively, in mice. IL-25, IL-33 and TSLP were reported to be important for group 2 innate lymphoid cell (ILC2)-, but not Th2 cell-, dependent airway eosinophilia in a certain model using chitin beads. Here, we show that—in our murine models—epithelial cell-derived IL-33 and TSLP, but not IL-25, were crucial for activation of resident lung Th2 cells as well as group 2 innate lymphoid cells (ILC2s) to produce IL-5, resulting in development of chitin-induced airway eosinophilia. Our findings provide further insight into the underlying mechanisms of development of HDM-mediated allergic disorders.Ken AraeMasashi IkutaniKotaro HoriguchiSachiko YamaguchiYouji OkadaHiroki SugiyamaKeisuke OrimoHideaki MoritaHajime SutoKo OkumuraHaruhiko TaguchiKenji MatsumotoHirohisa SaitoKatsuko SudoSusumu NakaeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021) |
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Medicine R Science Q Ken Arae Masashi Ikutani Kotaro Horiguchi Sachiko Yamaguchi Youji Okada Hiroki Sugiyama Keisuke Orimo Hideaki Morita Hajime Suto Ko Okumura Haruhiko Taguchi Kenji Matsumoto Hirohisa Saito Katsuko Sudo Susumu Nakae Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin |
| description |
Abstract Exposure to various antigens derived from house dust mites (HDM) is considered to be a risk factor for development of certain allergic diseases such as atopic asthma, atopic dermatitis, rhinitis and conjunctivitis. Chitin is an insoluble polysaccharide (β-(1–4)-poly-N-acetyl-d-glucosamine) and a major component in the outer shell of HDMs. Mice exposed to chitin develop asthma-like airway eosinophilia. On the other hand, several lines of evidence show that the effects of chitin on immune responses are highly dependent on the size of chitin particles. In the present study, we show that chitin induced production of IL-33 and TSLP by alveolar and bronchial epithelial cells, respectively, in mice. IL-25, IL-33 and TSLP were reported to be important for group 2 innate lymphoid cell (ILC2)-, but not Th2 cell-, dependent airway eosinophilia in a certain model using chitin beads. Here, we show that—in our murine models—epithelial cell-derived IL-33 and TSLP, but not IL-25, were crucial for activation of resident lung Th2 cells as well as group 2 innate lymphoid cells (ILC2s) to produce IL-5, resulting in development of chitin-induced airway eosinophilia. Our findings provide further insight into the underlying mechanisms of development of HDM-mediated allergic disorders. |
| format |
article |
| author |
Ken Arae Masashi Ikutani Kotaro Horiguchi Sachiko Yamaguchi Youji Okada Hiroki Sugiyama Keisuke Orimo Hideaki Morita Hajime Suto Ko Okumura Haruhiko Taguchi Kenji Matsumoto Hirohisa Saito Katsuko Sudo Susumu Nakae |
| author_facet |
Ken Arae Masashi Ikutani Kotaro Horiguchi Sachiko Yamaguchi Youji Okada Hiroki Sugiyama Keisuke Orimo Hideaki Morita Hajime Suto Ko Okumura Haruhiko Taguchi Kenji Matsumoto Hirohisa Saito Katsuko Sudo Susumu Nakae |
| author_sort |
Ken Arae |
| title |
Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin |
| title_short |
Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin |
| title_full |
Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin |
| title_fullStr |
Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin |
| title_full_unstemmed |
Interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin |
| title_sort |
interleukin-33 and thymic stromal lymphopoietin, but not interleukin-25, are crucial for development of airway eosinophilia induced by chitin |
| publisher |
Nature Portfolio |
| publishDate |
2021 |
| url |
https://doaj.org/article/b2ff8b41fa784b708de791905ef9f743 |
| work_keys_str_mv |
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| _version_ |
1718395722176397312 |