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Oligosaccharide‐dependent anti‐inflammatory role of galectin‐1 for macrophages in ulcerative colitis
Author(s) -
Iwatani Shuko,
Shinzaki Shinichiro,
Amano Takahiro,
Otake Yuriko,
Tani Mizuki,
Yoshihara Takeo,
Tsujii Yoshiki,
Hayashi Yoshito,
Inoue Takahiro,
Okuzaki Daisuke,
Mizushima Tsunekazu,
Miyoshi Eiji,
Iijima Hideki,
Takehara Tetsuo
Publication year - 2020
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.15097
Subject(s) - ulcerative colitis , colitis , galectin 1 , galectin 3 , medicine , inflammatory bowel disease , microbiology and biotechnology , galectin , immunology , cd64 , flow cytometry , pathology , biology , disease
Abstract Background and Aim Galectin‐1 plays a protective role against colitis by binding with polylactosamine structures on macrophages in β‐1,4‐galactosyltransferase I‐deficient mice, but the precise function of galectin‐1 remains unknown. In the present study, we investigated the anti‐inflammatory role of galectin‐1 on macrophages to ameliorate ulcerative colitis in both animal model and human tissue samples. Methods The expression of galectin‐1 in colonic tissues of ulcerative colitis patients was evaluated by immunohistochemistry. Cytokine production of mouse bone marrow‐derived macrophages (BMDMs) cultured with galectin‐1 was investigated. Galectin‐1 binding capacity and polylactosamine expression in macrophages stimulated with lipopolysaccharides were evaluated by flow cytometry. BMDMs cultured with galectin‐1 were transferred into Recombination activating gene (Rag) 2 −/− mice, and the severity of the dextran sodium sulfate‐induced colitis model was investigated. Furthermore, RNA sequencing was performed to characterize macrophages treated with galectin‐1. Results In ulcerative colitis patients, tissue expression of galectin‐1was decreased in inflamed mucosa compared with non‐inflamed mucosa. Galectin‐1 induced interleukin‐10 production in BMDMs, and the interleukin‐10 production was abrogated by lactose, which inhibits the interaction of oligosaccharide–galectin binding. Dextran sodium sulfate colitis was significantly ameliorated in Rag2 −/− mice undergoing galectin‐1‐treated BMDM transfer compared with those undergoing vehicle‐treated BMDM transfer. RNA sequencing revealed that treatment with galectin‐1 increased the expression of CCAAT/enhancer binding protein β and CD163, but decreased the expression of CD80 on BMDMs. Conclusion Galectin‐1, whose expression is decreased in the inflamed mucosa of ulcerative colitis patients, can ameliorate murine colitis by conferring oligosaccharide‐dependent anti‐inflammatory properties to macrophages.