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01.03.2016 | Original Research Paper

A critical role of Dectin-1 in hypersensitivity pneumonitis

verfasst von: Mari Higashino-Kameda, Toshiki Yabe-Wada, Shintaro Matsuba, Kazuya Takeda, Kazushi Anzawa, Takashi Mochizuki, Koichi Makimura, Shinobu Saijo, Yoichiro Iwakura, Hirohisa Toga, Akira Nakamura

Erschienen in: Inflammation Research | Ausgabe 3/2016

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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.

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Titel: A critical role of Dectin-1 in hypersensitivity pneumonitis
verfasst von: Mari Higashino-Kameda
Toshiki Yabe-Wada
Shintaro Matsuba
Kazuya Takeda
Kazushi Anzawa
Takashi Mochizuki
Koichi Makimura
Shinobu Saijo
Yoichiro Iwakura
Hirohisa Toga
Akira Nakamura
Publikationsdatum: 01.03.2016
Verlag: Springer International Publishing
Erschienen in: Inflammation Research / Ausgabe 3/2016
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI: https://doi.org/10.1007/s00011-015-0910-1

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Objectives and design

Materials and methods

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