KMID : 0988920180160030384
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Intestinal Research 2018 Volume.16 No. 3 p.384 ~ p.392
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¥â-(1,3)-Glucan derived from Candida albicans induces inflammatory cytokines from macrophages and lamina propria mononuclear cells derived from patients with Crohn¡¯s disease
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Mori Kiyoto
Naganuma Makoto Mizuno Shinta Suzuki Hiroaki Kitazume Mina T. Shimamura Katsuyoshi Chiba Sayako Sugita Akira Matsuoka Katsuyoshi Hisamatsu Tadakazu Kanai Takanori
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Abstract
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Background/Aims: Recent research has highlighted the importance of interactions between commensal fungi and intestinal inflammation. However, there are few studies investigating whether commensal fungi contribute to inflammation in patients with Crohn¡¯s disease (CD). The aim of this study is to investigate reveal interactions between commensal fungi and host immune cells in CD.
Methods: CD14-positive monocytes were isolated from peripheral blood mononuclear cells from healthy human volunteers and then differentiated in the presence of macrophage colony-stimulating factor (M-CSF) (referred to as M-macrophages, M-M¥õs) or M-CSF and interferon-¥ã (IFN-¥ã) (referred to as M-gamma macrophages, M¥ã-M¥õs). Cytokine production by these in vitro differentiated macrophages in response to ¥â-(1,3)-glucan was analyzed by flow cytometry. Expression of Dectin-1 was examined using flow cytometry, western blotting, and quantitative reverse transcription-polymerase chain reaction. Cytokine production by in vitro differentiated macrophages in response to ¥â-(1,3)-glucan was measured in the presence of an anti-Dectin-1 receptor antagonist, anti-Syr, or an anti-Fas-1 antibody. Cytokine production by lamina propria mononuclear cells (LPMCs) derived from CD patients in response to ¥â-(1,3)-glucan was also analyzed.
Results: M¥ã-M¥õs produced a large amount of tumor necrosis factor-¥á (TNF-¥á) and interleukin-6 in response to ¥â-(1,3)-glucan. Dectin-1 expression was significantly higher in M¥ã-M¥õs than in M-M¥õs. The increase in TNF-¥á production by M¥ã-M¥õs stimulated with glucan was reversed by blocking Dectin-1, Syr or Fas-1. LPMCs derived from CD patients stimulated with ¥â-(1,3)-glucan produced significantly higher amount of TNF-¥á than LPMCs derived from UC patients.
Conclusions: These results suggest that commensal fungal microbiota may contribute to the pathogenesis of CD by inducing macrophages-derived pro-inflammatory cytokines.
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KEYWORD
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Crohn disease, Candida albicans, Tumor necrosis factor-alpha, Dectin-1
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