Basic Gastronenterology最新文献

{"title":"IDDF2021-ABS-0098 Comparison of curative effect between metformin and mesalazine in the treatment of experimental colitis","authors":"Jun Deng, Lishan Zeng, Le Liu, Ye Chen","doi":"10.1136/gutjnl-2021-iddf.35","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.35","url":null,"abstract":"Background To evaluate the different efficacy in the treatment of mice colitis between metformin and mesalazine.","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116988996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0054 Appendectomy increases the risk of colorectal cancer through causing gut microbiota dysbiosis in a large population-based study","authors":"F. Shi, Gaixia Liu, Yufeng Lin, Cosmos liutao Guo, Jing Han, J. She","doi":"10.1136/gutjnl-2021-iddf.24","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.24","url":null,"abstract":"IDDF2021-ABS-0054 Figure 1 Abstract IDDF2021-ABS-0054 Figure 2 Abstracts Gut 2021;70(Suppl 2):A1–A150 A17 on D ecem er 8, 2022 by gest. P rocted by coright. http/gut.bm jcom / G t: frst pulished as 10.113utjnl-2021-ID D F 24 on 2 S etem er 221. D ow nladed fom","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"48 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126780484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0068 Removal of host dna from tissue biopsies improves detection sensitivity of gut microbiota by shotgun metagenomic sequencing","authors":"W. Cheng","doi":"10.1136/gutjnl-2021-iddf.28","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.28","url":null,"abstract":"","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125757337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0061 TM9SF4 ameliorates inflammatory bowel disease by alleviating inflammation and er stress in colonic epithelial cells and macrophages","authors":"Mingxu Xie, Hongyan Yu, W. Ko, W. Mak, Xiaoqiang Yao","doi":"10.1136/gutjnl-2021-iddf.25","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.25","url":null,"abstract":"","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133281661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0140 Gut microbiota significantly correlate with body constitution in traditional chinese medicine","authors":"Haohui Liu, Meihui Xu, K. Toh, C. Chong, J. Lim, J. W. Lee","doi":"10.1136/gutjnl-2021-iddf.45","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.45","url":null,"abstract":"","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"46 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130154509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0189 Metabolic inhibitor of PFKFB3 and its implication in immune evasion by upregulating pd-l1 expression via the PHOSPHOPFKFB3–HIF1Α–PD-L1 axis","authors":"Jianliang Zheng","doi":"10.1136/gutjnl-2021-iddf.53","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.53","url":null,"abstract":"Background PFKFB3 is a crucial metabolic enzyme which is highly upregulated in cancer cells, prompting much research on potential selective inhibitors of PFKFB3 which all have shown promising tumor inhibitive effects. However, clinical trials such as NCT02044861 on PFKFB3 inhibitors seem resultless. With recent implications of cancer metabolism and tumor immune evasion, we hypothesized that PFKFB3 inhibition and subsequent metabolic reprogramming might affect tumor immune evasion. Methods We examined the function of PFK-15 on tumor cells in vitro and in vivo in immune-deficient nude-mice models and immune-competent mouse models such as C57/BALB/c-CDX models and huPBMC-CDX and PBX models. CO-IP, fluorescent immunohistochemistry, CHIP and dual-luciferase assays were used to investigate the underlying mechanism. Results Inhibition of PFKFB3 using PFK-15 suppressed cell growth in human esophageal cell lines in vitro and in vivo in immune-deficient xenografts. However, inhibition of PFKFB3 caused a marked upregulation in PD-L1 which inactivated cocultured T-cells in vitro and compromised anti-tumor immunity in immune-competent mouse, an effect which could be reversed when PFK-15 was combined with PD-1 mab. Mechanistically, we identified ERK pathway upregulation after treatment with PFK-15, which increased PFKFB3 phosphorylation levels, causing its transformation and increased its binding with HIF-1α, then Phospho-PFKFB3 co-translocated into the nucleus together with HIF-1α by binding with importin α5, whereby nuclear HIF-1α attaches itself to HRE regions on PD-L1 promoter, upregulating PD-L1 expression. Clinically, we observed higher Phospho-PFKFB3 in tumor tissues from non-responders to PD-1 mab treated ESCC patients. Conclusions This study shows that inhibition of PFKFB3 increases immune evasion via the phospho-PFKFB3–HIF-1α–PD-L1 axis. The translational significance of this study lies in the fact that in-vivo experiments in immune-competent mice using the closest to human immune tumor microenvironment model huPBMC-CDX/PDX combining PFKFB3 inhibitors and PD-1 mab resulted in a marked decrease in tumor development. These findings may be of relevance for the design of anti-cancer treatment trials with PFKFB3 inhibitors.","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"40 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116391426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0183 SLC25A22 drives immune suppression in kras-mutant colorectal cancer","authors":"Qiming Zhou, Yao Peng, Lam-Shing Chen, Huarong Chen, W. Kang, Yuqiang Nie, Jun Yu, C. Wong","doi":"10.1136/gutjnl-2021-iddf.51","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.51","url":null,"abstract":"Background Direct targeting of KRAS is challenging and represents an unmet need. We identified SLC25A22, a mitochondrial glutamate transporter, as a potential therapeutic target in KRAS mutant colorectal cancer (CRC). In this study, we reveal that SLC25A22 underlies mutant KRAS-induced immune suppression in CRC. Methods Immune cell infiltration was determined by flow cytometry. The immunosuppressive effect and migration of MDSC were estimated by T cell suppression assay and transwell assay, respectively. Results Tumors from ApcMin/+KrasG12DVillin-Cre mice demonstrated marked infiltration in immunosuppressive myeloid-derived suppressor cells (MDSC) (P (IDDF2021-ABS-0183 Figure 5. SLC25A22 recruits MDSC migration via CXCL1/CXCR2 axis, IDDF2021-ABS-0183 Figure 6. SLC25A22 recruits MDSC migration via CXCL1/CXCR2 axis) Conclusions Our work suggests a SLC25A22-chemokine axis that promotes an immune suppressive microenvironment in KRAS-mutant CRC and implies that SLC25A22 constitutes a novel target for immunotherapies.","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"545 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116491746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0066 Antioxidants-rich supplements increase faecalibacterium abundance in gut microbiota","authors":"Bangwei Chen, Chuyao Wang, Zhiming Li, Tao Li","doi":"10.1136/gutjnl-2021-iddf.27","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.27","url":null,"abstract":"","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"17 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131769623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0076 lncRNA TNFRSF10A-AS1 mediates tumorigenesis of gastric cancer by directly binding to MPZL1 and associates with patient outcomes","authors":"Donglei Sun, Hongyan Gou, Dandan Wang, Jun Yu","doi":"10.1136/gutjnl-2021-iddf.32","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.32","url":null,"abstract":"Background LncRNA was known to be closely associated with the progression of human tumors. The role of new lncRNA TNFRSF10A-AS1 in the pathogenesis and progression of gastric tumor is still unclear. The aim of this study was to investigate the function of TNFRSF10A-AS1 and the underlying mechanism in the pathogenesis and progression of gastric cancer. Methods The clinical impact of TNFRSF10A-AS1 was assessed in 105 patients with gastric cancer. The biological function of TNFRSF10A-AS1 was studied in vitro and in vivo. TNFRSF10A-AS1 downstream effector were identified by RNA FISH, RNA sequencing, RNA pulldown and rescue assay. Results TNFRSF10A-AS1was upregulated in gastric cancer cell lines and tissues. Multivariate analysis showed that gastric cancer patients with TNFRSF10A-AS1 overexpression had a significantly shortened survival. TNFRSF10A-AS1 significantly promoted gastric cancer cell proliferation, cell-cycle transformation, and migration/invasion, but suppressed cell apoptosis. Silencing TNFRSF10A-AS1 expression exerted opposite effects in vitro and significantly inhibited xenograft tumor growth in nude mice. Mechanically, TNFRSF10A-AS1 directly bound to MPZL1 and activated MPZL1 transcription. Knockdown MPZL1 abrogated the effect of TNFRSF10A-AS1 in the tumor-promoting function. Conclusions TNFRSF10A-AS1 directly binds to oncogenic MPZL1 to induce its expression. TNFRSF10A-AS1 plays a pivotal oncogenic role in gastric carcinogenesis and is an independent prognostic factor for gastric cancer patients.","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"143 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124012415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IDDF2021-ABS-0069 Ecology and network analyses for the fecal microbiome in ulcerative colitis (UC)","authors":"Yang Sun, Yinglei Miao","doi":"10.1136/gutjnl-2021-iddf.29","DOIUrl":"https://doi.org/10.1136/gutjnl-2021-iddf.29","url":null,"abstract":"","PeriodicalId":399396,"journal":{"name":"Basic Gastronenterology","volume":"155 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114511575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}