IL-33, IL-25 and TSLP contribute to development of fungal-associated protease-induced innate-type airway inflammation
| Autor: | Susumu Nakae, Takamichi Yoshizaki, Seiko Narushima, Eri Shimura, Kenji Matsumoto, Motoyasu Iikura, Tomoaki Hoshino, Sachiko Yamaguchi, Maho Suzukawa, Akira Matsuda, Hajime Suto, Yasuhiro Yamauchi, Takafumi Numata, Ken Arae, Wakako Nakanishi, Katsuko Sudo, Hideaki Morita, Ayako Takamori, Hirohisa Saito, Ko Okumura, Yoshihisa Hiraishi, Aya Nambu, Takahide Nagase, Yosuke Asada |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Proteases Thymic stromal lymphopoietin lcsh:Medicine Biology Article 03 medical and health sciences Mice 0302 clinical medicine Immune system Thymic Stromal Lymphopoietin medicine Eosinophilia Animals Pulmonary Eosinophilia lcsh:Science Mice Knockout Immunity Cellular Multidisciplinary Innate immune system Lung Diseases Fungal Interleukins Innate lymphoid cell lcsh:R Pneumonia Allergens respiratory system Interleukin-33 Immunity Innate respiratory tract diseases Interleukin 33 Mice Inbred C57BL TLR2 030104 developmental biology Aspergillus Immunology Cytokines lcsh:Q medicine.symptom 030215 immunology Peptide Hydrolases |
| Zdroj: | Scientific Reports, Vol 8, Iss 1, Pp 1-12 (2018) Scientific Reports |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/s41598-018-36440-x |
| Popis: | Certain proteases derived from house dust mites and plants are considered to trigger initiation of allergic airway inflammation by disrupting tight junctions between epithelial cells. It is known that inhalation of proteases such as house dust mite-derived Der p1 and/or papaya-derived papain caused airway eosinophilia in naïve mice and even in Rag-deficient mice that lack acquired immune cells such as T, B and NKT cells. In contrast, little is known regarding the possible involvement of proteases derived from Aspergillus species (fungal-associated proteases; FAP), which are ubiquitous saprophytic fungi in the environment, in the development of allergic airway eosinophilia. Here, we found that inhalation of FAP by naïve mice led to airway eosinophilia that was dependent on protease-activated receptor-2 (PAR2), but not TLR2 and TLR4. Those findings suggest that the protease activity of FAP, but not endotoxins in FAP, are important in the setting. In addition, development of that eosinophilia was mediated by innate immune cells (ILCs) such as innate lymphoid cells, but not by acquired immune cells such as T, B and NKT cells. Whereas IL-33, IL-25 and thymic stromal lymphopoietin (TSLP) are involved in induction of FAP-induced ILC-mediated airway eosinophilia, IL-33—rather than IL-25 and/or TSLP—was critical for the eosinophilia in our model. Our findings improve our understanding of the molecular mechanisms involved in induction of airway inflammation by FAP. |
| Databáze: | OpenAIRE |
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