Anti-HBV drug entecavir ameliorates DSS-induced colitis through PD-L1 induction
PD-L1-mediated signaling is one of the major processes that regulate local inflammatory responses in the gut. To date, protective effects against colitis through direct Fc-fused PD-L1 administration or indirect PD-L1 induction by probiotics have been reported. We have previously shown that the anti-...
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| Published in | Pharmacological research Vol. 179; p. 105918 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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01.05.2022
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| Abstract | PD-L1-mediated signaling is one of the major processes that regulate local inflammatory responses in the gut. To date, protective effects against colitis through direct Fc-fused PD-L1 administration or indirect PD-L1 induction by probiotics have been reported. We have previously shown that the anti-HBV drug entecavir (ETV) induces PD-L1 expression in human hepatocytes. In the present study, we investigated whether ETV induces PD-L1 expression in intestinal cells and provides a protective effect against DSS-induced colitis. ETV induced PD-L1 expression in epithelial cells, rather than T and B cells, improving the symptoms of colitis. In the mechanistic analysis, Th17 cell differentiation was inhibited and B cell infiltration into the lamina propria was reduced. In addition, PD-L1 expression was positively correlated with Foxp3 or CSF1-R. In conclusion, ETV upregulated PD-L1 expression in epithelial cells and ameliorated inflammation in DSS-induced colitis. These results suggest that ETV may be a potential therapeutic agent as a PD-L1 enhancer for the treatment of human IBD.
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| AbstractList | PD-L1-mediated signaling is one of the major processes that regulate local inflammatory responses in the gut. To date, protective effects against colitis through direct Fc-fused PD-L1 administration or indirect PD-L1 induction by probiotics have been reported. We have previously shown that the anti-HBV drug entecavir (ETV) induces PD-L1 expression in human hepatocytes. In the present study, we investigated whether ETV induces PD-L1 expression in intestinal cells and provides a protective effect against DSS-induced colitis. ETV induced PD-L1 expression in epithelial cells, rather than T and B cells, improving the symptoms of colitis. In the mechanistic analysis, Th17 cell differentiation was inhibited and B cell infiltration into the lamina propria was reduced. In addition, PD-L1 expression was positively correlated with Foxp3 or CSF1-R. In conclusion, ETV upregulated PD-L1 expression in epithelial cells and ameliorated inflammation in DSS-induced colitis. These results suggest that ETV may be a potential therapeutic agent as a PD-L1 enhancer for the treatment of human IBD. PD-L1-mediated signaling is one of the major processes that regulate local inflammatory responses in the gut. To date, protective effects against colitis through direct Fc-fused PD-L1 administration or indirect PD-L1 induction by probiotics have been reported. We have previously shown that the anti-HBV drug entecavir (ETV) induces PD-L1 expression in human hepatocytes. In the present study, we investigated whether ETV induces PD-L1 expression in intestinal cells and provides a protective effect against DSS-induced colitis. ETV induced PD-L1 expression in epithelial cells, rather than T and B cells, improving the symptoms of colitis. In the mechanistic analysis, Th17 cell differentiation was inhibited and B cell infiltration into the lamina propria was reduced. In addition, PD-L1 expression was positively correlated with Foxp3 or CSF1-R. In conclusion, ETV upregulated PD-L1 expression in epithelial cells and ameliorated inflammation in DSS-induced colitis. These results suggest that ETV may be a potential therapeutic agent as a PD-L1 enhancer for the treatment of human IBD.PD-L1-mediated signaling is one of the major processes that regulate local inflammatory responses in the gut. To date, protective effects against colitis through direct Fc-fused PD-L1 administration or indirect PD-L1 induction by probiotics have been reported. We have previously shown that the anti-HBV drug entecavir (ETV) induces PD-L1 expression in human hepatocytes. In the present study, we investigated whether ETV induces PD-L1 expression in intestinal cells and provides a protective effect against DSS-induced colitis. ETV induced PD-L1 expression in epithelial cells, rather than T and B cells, improving the symptoms of colitis. In the mechanistic analysis, Th17 cell differentiation was inhibited and B cell infiltration into the lamina propria was reduced. In addition, PD-L1 expression was positively correlated with Foxp3 or CSF1-R. In conclusion, ETV upregulated PD-L1 expression in epithelial cells and ameliorated inflammation in DSS-induced colitis. These results suggest that ETV may be a potential therapeutic agent as a PD-L1 enhancer for the treatment of human IBD. PD-L1-mediated signaling is one of the major processes that regulate local inflammatory responses in the gut. To date, protective effects against colitis through direct Fc-fused PD-L1 administration or indirect PD-L1 induction by probiotics have been reported. We have previously shown that the anti-HBV drug entecavir (ETV) induces PD-L1 expression in human hepatocytes. In the present study, we investigated whether ETV induces PD-L1 expression in intestinal cells and provides a protective effect against DSS-induced colitis. ETV induced PD-L1 expression in epithelial cells, rather than T and B cells, improving the symptoms of colitis. In the mechanistic analysis, Th17 cell differentiation was inhibited and B cell infiltration into the lamina propria was reduced. In addition, PD-L1 expression was positively correlated with Foxp3 or CSF1-R. In conclusion, ETV upregulated PD-L1 expression in epithelial cells and ameliorated inflammation in DSS-induced colitis. These results suggest that ETV may be a potential therapeutic agent as a PD-L1 enhancer for the treatment of human IBD. [Display omitted] |
| ArticleNumber | 105918 |
| Author | Roncador, Giovanna Carreras, Joaquim Kikuti, Yara Yukie Kakizaki, Masatoshi Nakamura, Naoya Shimizu, Takanobu Yamamoto, Yuichiro Kotani, Ai |
| Author_xml | – sequence: 1 givenname: Yuichiro surname: Yamamoto fullname: Yamamoto, Yuichiro organization: Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, Isehara 259-1193, Japan – sequence: 2 givenname: Joaquim orcidid: 0000-0002-6129-8299 surname: Carreras fullname: Carreras, Joaquim organization: Department of Pathology, Tokai University School of Medicine, Isehara 259-1193, Japan – sequence: 3 givenname: Takanobu surname: Shimizu fullname: Shimizu, Takanobu organization: Department of Innovative Medical Science, Tokai University School of Medicine, Isehara 259-1193, Japan – sequence: 4 givenname: Masatoshi surname: Kakizaki fullname: Kakizaki, Masatoshi organization: Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, Isehara 259-1193, Japan – sequence: 5 givenname: Yara Yukie surname: Kikuti fullname: Kikuti, Yara Yukie organization: Department of Pathology, Tokai University School of Medicine, Isehara 259-1193, Japan – sequence: 6 givenname: Giovanna surname: Roncador fullname: Roncador, Giovanna organization: Monoclonal Antibodies Unit, Spanish National Cancer Research Institute (CNIO), Melchor Fernandez Almagro 3, 28029 Madrid, Spain – sequence: 7 givenname: Naoya surname: Nakamura fullname: Nakamura, Naoya organization: Department of Pathology, Tokai University School of Medicine, Isehara 259-1193, Japan – sequence: 8 givenname: Ai surname: Kotani fullname: Kotani, Ai email: aikotani@k-lab.jp organization: Division of Hematological Malignancy, Institute of Medical Sciences, Tokai University, Isehara 259-1193, Japan |
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| Keywords | GALT FFPET LP IHC ETV HRP Entecavir IBD IL-22 SLE MFI S1P Th17 Cell Treg Cell PD-L1 HBV NRTI Th17 CD GI DSS CD19 + B cell CSF1-R H&E Treg IL-10 TNF-α JAK mAbs TGF-β1 Foxp3 PD-1 HDAC |
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