Mari Higashino-Kameda1,2, Toshiki Yabe-Wada2, Shintaro Matsuba2, Kazuya Takeda2, Kazushi Anzawa3, Takashi Mochizuki3, Koichi Makimura4, Shinobu Saijo5, Yoichiro Iwakura6, Hirohisa Toga1, Akira Nakamura7. 1. Department of Respiratory Medicine, Kanazawa Medical University, Uchinada, Ishikawa, Japan. 2. Department of Immunology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa Prefecture, 920-0293, Japan. 3. Department of Dermatology, Kanazawa Medical University, Uchinada, Ishikawa, Japan. 4. Laboratory of Space and Environmental Medicine, Teikyo University, Hachioji, Tokyo, Japan. 5. Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan. 6. Center for Animal Disease Models, Research Institute for Biological Sciences, Tokyo University of Science, Noda, Chiba, Japan. 7. Department of Immunology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa Prefecture, 920-0293, Japan. aki-n@kanazawa-med.ac.jp.
Abstract
OBJECTIVES AND DESIGN: Hypersensitivity pneumonitis (HP) is a pulmonary disease caused by repeated exposure to various aspiration antigens, including bacteria and fungi. Although TLRs are known to be required for the generation of HP triggered by bacteria, the significance of fungal receptors remains unclear. The present study aimed to investigate whether Dectin-1 and Dectin-2 contribute to the development of experimental HP triggered by the fungus Trichosporon asahii (T. asahii) that causes summer-type HP. MATERIALS AND METHODS: We investigated the binding between Dectin-Fc protein and T. asahii by a dot blot assay. We performed the histological and flow cytometric analysis in the HP model using Dectin-1-deficient (Dectin-1(-/-)) and Dectin-2(-/-) mice. We also investigated Th17/Th1 responses in lung cells, and measured an IL-17-promoting cytokine IL-23 from bone marrow-derived dendritic cells (BMDCs) by ELISA. RESULTS: Dectin-1 bound more strongly to T. asahii than Dectin-2. Dectin-1(-/-) mice barely developed HP, whereas both wild-type mice and Dectin-2(-/-) mice developed similar lung diseases. Dectin-1 deficiency decreased the infiltration of neutrophils and monocyte-derived macrophages and repressed the expansion of lung CD4(+)IL-17A(+) cells. The production of IL-23 p19 was reduced in Dectin-1(-/-) BMDCs. CONCLUSIONS: These data suggested Dectin-1 plays a critical role in the development of fungus-induced HP.
OBJECTIVES AND DESIGN:Hypersensitivitypneumonitis (HP) is a pulmonary disease caused by repeated exposure to various aspiration antigens, including bacteria and fungi. Although TLRs are known to be required for the generation of HP triggered by bacteria, the significance of fungal receptors remains unclear. The present study aimed to investigate whether Dectin-1 and Dectin-2 contribute to the development of experimental HP triggered by the fungus Trichosporon asahii (T. asahii) that causes summer-type HP. MATERIALS AND METHODS: We investigated the binding between Dectin-Fc protein and T. asahii by a dot blot assay. We performed the histological and flow cytometric analysis in the HP model using Dectin-1-deficient (Dectin-1(-/-)) and Dectin-2(-/-) mice. We also investigated Th17/Th1 responses in lung cells, and measured an IL-17-promoting cytokine IL-23 from bone marrow-derived dendritic cells (BMDCs) by ELISA. RESULTS:Dectin-1 bound more strongly to T. asahii than Dectin-2. Dectin-1(-/-) mice barely developed HP, whereas both wild-type mice and Dectin-2(-/-) mice developed similar lung diseases. Dectin-1deficiency decreased the infiltration of neutrophils and monocyte-derived macrophages and repressed the expansion of lung CD4(+)IL-17A(+) cells. The production of IL-23 p19 was reduced in Dectin-1(-/-) BMDCs. CONCLUSIONS: These data suggested Dectin-1 plays a critical role in the development of fungus-induced HP.
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