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| 1 | Contribution of the IL-17/IL-23 axis to the pathogenesis of inflammatory bowel disease显示文摘Inflammatory bowel diseases(IBDs) are chronic disorders of modern society, requiring management strategies aimed at prolonging an active life and establishing the exact etiology and pathogenesis.These idiopathic diseases have environmental, genetic,immunologic, inflammatory, and oxidative stress components. On the one hand, recent advances have shown that abnormal immune reactions against the microorganisms of the intestinal flora are responsible for the inflammation in genetically susceptible individuals. On the other hand, in addition to T helper cell-type(Th) 1 and Th2 immune responses,other subsets of T cells, namely regulatory T cells and Th17 maintained by IL-23 are likely to develop IBD. IL-23 acts on innate immune system members and also facilitates the expansion and maintenance of Th17 cells. The IL-17/IL-23 axis is relevant in IBD pathogenesis both in human and experimental studies. Novel biomarkers of IBD could be calprotectin,microRNAs, and serum proinflammatory cytokines.An efficient strategy for IBD therapy is represented by the combination of IL-17 A and IL-17 F in acute IL-17 A knockout TNBS-induced colitis, and also definite decrease of the inflammatory process in IL-17 F knockout, DSS-induced colitis have been observed.Studying the correlation between innate and adaptive immune systems, we hope to obtain a focused reviewin order to facilitate future approaches aimed at elucidating the immunological mechanisms that control gut inflammation. | Cristina-Sorina Cǎanǎ Ioana Berindan Neagoe Vasile Cozma Cristian Magdas Flaviu Tǎbǎan Dan Lucian Dumitrasu | 2015 | World Journal of Gastroenterology2015，21，19： | 37 |
| 2 | 炎症性肠病发病机制的研究新进展显示文摘炎症性肠病(inflammatory bowel disease,IBD)是一组反复发作的慢性炎症性肠道疾病,主要包括溃疡性结肠炎(ulcerative colitis,UC)和克罗恩病(Crohn’s disease,CD)。其确切的发病机制目前尚不明确,本文主要对遗传因素、免疫因素、环境因素、内质网应激和肠道微生物这五个方面在IBD中的新观点作一概述。 | 余世界 董卫国 | 2014 | 胃肠病学和肝病学杂志2014，23，2： | 17 |
| 3 | Etiology of inflammatory bowel disease:A unified hypothesis显示文摘Inflammatory bowel disease(IBD),including both ulcerative colitis(UC) and Crohn's disease(CD),emerged and dramatically increased for about a century.Despite extensive research,its cause remains regarded as unknown.About a decade ago,a series of findings made me suspect that saccharin may be a key causative factor for IBD,through its inhibition on gut bacteria and the resultant impaired inactivation of digestive proteases and over digestion of the mucus layer and gut barrier(the Bacteria-Protease-Mucus-Barrier hypothesis).It explained many puzzles in IBD such as its emergence and temporal changes in last century.Recently I further found evidence suggesting sucralose may be also linked to IBD through a similar mechanism as saccharin and have contributed to the recent worldwide increase of IBD.This new hypothesis suggests that UC and CD are just two symptoms of the same morbidity,rather than two different diseases.They are both caused by a weakening in gut barrier and only differ in that UC is mainly due to increased infiltration of gut bacteria and the resultant recruitment of neutrophils and formation of crypt abscess,while CD is mainly due to increased infiltration of antigens and particles from gut lumen and the resultant recruitment of macrophages and formation of granulomas.It explained the delayed appearance but accelerated increase of CD over UC and many other phenomena.This paper aims to provide a detailed description of a unified hypothesis regardingthe etiology of IBD,including the cause and mechanism of IBD,as well as the relationship between UC and CD. | Xiaofa Qin | 2012 | World Journal of Gastroenterology2012，18，15： | 13 |
| 4 | Association of fucosyltransferase 2 gene variants with ulcerative colitis in Han and Uyghur patients in China显示文摘AIM:To investigate the contribution of fucosyltransferase 2 (FUT2) variants to the genetic susceptibility and clinical heterogeneity of ulcerative colitis (UC) between Han and Uyghur patients in Xinjiang, China. METHODS:A total of 102 UC patients (53 Han patients including 22 men and 31 women, and 49 Uyghur patients including 25 men and 24 women; aged 48 ± 16 years) and 310 age-and sex-matched healthy controls were enrolled from January 2010 to May 2011 in Xinjiang People's Hospital of China. UC was diagnosed based on the clinical, endoscopic and histological findings following Lennard-Jones criteria. Blood samples were collected and genomic DNA was extracted by the routine laboratory methods. Polymerase chain reaction-sequence-based typing method was used to identify FUT2 variants rs281377, rs1047781, rs601338 and rs602662. Genotypic and allelic frequencies were documented and compared between the UC patients and the healthy controls. Genotypic frequencies were also compared between Han and Uyghur patients. Potential association of genetic variation and UC between Han and Uyghur patients was examined. RESULTS: rs281377 was found significantly associated with UC in the Han population as compared with the controls (P = 0.011) while rs281377 was not associated with UC in the Uyghur population (P = 0.06). TT homozygous rs281377 frequencies were higher in the UC groups than in the controls (88.7% vs 68.7% and 55.1% vs 50.3%). rs1047781 was specifically associated with UC in the Uyghur population (P = 0.001), but not associated with UC in the Han population (P = 0.13). TT homozygous rs1047781 frequencies were lower in the UC groups than in the controls (9.5% vs 11.8% and 4.0% vs 6.7%). rs601338 was statistically related to UC in both populations (Han, P = 0.025; Uyghur, P = 8.33 × 10 -5 ). AA homozygous rs601338 frequencies were lower in the UC groups than in the controls (0% vs 1.8% and 12.2% vs 13.4%). No association was found between rs602662 and UC in both Han and the Uyghur populations. Allelic analysis showed that rs281377 allele was significantly associated with UC in the Han population as compared with the controls [P = 0.001, odd ratio (OR) = 0.26], however, it was not associated with UC in the Uyghur population (P = 0.603, OR = 1.14), and rs1047781 allele was associated with UC in the Uyghur population (P = 0.001, OR = 0.029) while it was not associated with UC in the Han population (P = 0.074, OR = 0.62). Moreover, rs601338 was associated with UC in both Han (P = 0.005, OR = 0.1) and Uyghur pop- ulations (P = 0.002, OR = 0.43). Meta analysis showed that rs1047781 and rs601338 conferred risk of UC as compared with the controls [P = 0.005, OR = 0.47; P = 0.0003, OR = 0.35; 95% confidence interval (CI) = 0.31-0.72 and 0.21-0.58], but rs281377 and rs602662 showed no statistically significant differences betweenpatients with UC and controls (P = 0.10, OR = 0.71; P = 0.68, OR = 0.09; 95% CI = 0.47-1.07 and 0.56-1.47). CONCLUSION:Functionally relevant FUT2 gene variants are associated with UC, suggesting that they play a potential role in the pathogenesis of UC and may contribute to the clinical heterogeneity of UC between Han and Uyghur patients. | Ayinuer Aheman He-Sheng Luo Feng Gao | 2012 | World Journal of Gastroenterology2012，18，34： | 9 |
| 5 | Gastrointestinal neuroendocrine peptides/amines in inflammatory bowel disease显示文摘Inflammatory bowel disease(IBD) is a chronic recurrent condition whose etiology is unknown,and it includes ulcerative colitis,Crohn's disease,and microscopic colitis. These three diseases differ in clinical manifestations,courses,and prognoses. IBD reduces the patients' quality of life and is an economic burden to both the patients and society. Interactions between the gastrointestinal(GI) neuroendocrine peptides/amines(NEPA) and the immune system are believed to play an important role in the pathophysiology of IBD. Moreover,the interaction between GI NEPA and intestinal microbiota appears to play also a pivotal role in the pathophysiology of IBD. This review summarizes the available data on GI NEPA in IBD,and speculates on their possible role in the pathophysiology and the potential use of this information when developing treatments. GI NEPA serotonin,the neuropeptide Y family,and substance P are proinflammatory,while the chromogranin/secretogranin family,vasoactive intestinal peptide,somatostatin,and ghrelin are antiinflammatory. Several innate and adaptive immune cells express these NEPA and/or have receptors to them. The GI NEPA are affected in patients with IBD and in animal models of human IBD. The GI NEPA are potentially useful for the diagnosis and follow-up of the activity of IBD,and are candidate targets for treatments of this disease. | Magdy El-Salhy Tefera Solomon Trygve Hausken Odd Helge Gilja Jan Gunnar Hatlebakk | 2017 | World Journal of Gastroenterology2017，23，28： | 8 |
| 6 | 维生素D与胃肠道疾病显示文摘维生素D在钙磷内稳态中起着关键的内分泌作用,而且维生素D还参与宿主防御、炎症、免疫调节和修复等一系列病理、生理过程。近年来研究发现维生素D缺乏与许多胃肠道疾病有关,如炎症性肠病、大肠癌、胃癌等。本文就维生素D与胃肠道疾病的相关研究进行综述。 | 马卫宁 洪建国 | 2014 | 医学研究杂志2014，43，12： | 8 |
| 7 | 内皮素-1在炎症性肠病发病中作用的研究进展显示文摘炎症性肠病(IBD)是一种病因尚未完全明确的慢性非特异性肠道炎性疾病,包括克罗恩病(CD)和溃疡性结肠炎(UC)。内皮素-1(ET-1)是一种由21个氨基酸残基组成的活性多肽,具有较强的收缩力,可通过活化血管平滑肌的电位依赖性钙离子通道发挥收缩血管作用。研究显示ET-1在IBD的发生、发展中发挥重要作用。本文就ET-1在IBD发病中作用的研究进展作一综述。 | 安博然 祝斌 | 2016 | 胃肠病学2016，21，5： | 5 |
| 8 | 新疆维吾尔族及汉族溃疡性结肠炎患者岩藻糖基转移酶2基因多态性差异初探显示文摘目的初步评估新疆维吾尔自治区汉族及维吾尔族UC患者的岩藻糖基转移酶2(FUT2)基因多态性的差异。方法纳入120例UC患者,其中汉族64例,维吾尔族56例,另有320名年龄、性别、民族相匹配的健康对照者。提取所有受试者的DNA,采用PCR扩增并测序,以确定F1,T2基因C357T、A385T、G428A、G739A的多态性,采用卡方检验比较汉族及维吾尔族UC患者与健康对照者的基因频率。结果C357T变异在汉族UC患者中的基因频率为CC0、CT 11.3%、TT88.7%,在相应的健康对照者中为CC5.5%、CT26.1%、TT68.4%(X^2=9.091,P=0.011)。A385T变异在维吾尔族UC患者中的基因频率为AA87.8%、AT8.2%、TT4.0%,在相n应的健康对照者中为AA59.7%、AT33.6%、TT6.7%(X^2=13.480,P=0.010)。G428A变异在汉族UC患者中的基因频率为GG98.1%、AG1.9%、AA0,在相应的健康对照者中为GG83.9%、nAG14.3%、AA1.8%()[。=7.382,P=0.025);C-428A变异在维吾尔族UC患者中的基因频率为GG69.4%、AG18.4%、AA12.2%,在相应的健康对照者中为GG35.6%、AG51.0%、AA13.4%。(X^2=18.790,P〈0.01)。G739A变异在汉族及维吾尔族Uc患者与相应的健康对照者中的基因频率差异均无统计学意义(P均〉0.05)。结论FuT2基因多态性与UC相关,其中在汉族人群中C357T、G428A与UC相关,在维吾尔族人群中A385T、G428A与UC相关,表明FuT2基因在新疆地区UC发病中可能起潜在作用。 | 阿依努尔·阿合曼 高峰 刘兴 艾合买江·库尔班江 黄晓玲 李莉 木尼拉·买买提 赫晓磊 | 2013 | 中华消化杂志2013，33，7： | 3 |
| 9 | 胆维丁乳对酵母多糖所致多器官功能障碍综合征小鼠肾脏作用的研究显示文摘目的研究胆维丁乳对酵母多糖所致多器官功能障碍综合征小鼠肾脏的作用。方法选取C57BL/6源性的野生小鼠36只,随机分为对照组、胆维丁乳组、酵母多糖组、胆维丁乳+酵母多糖组,每组9只,室温饲养,按组别分别自由饮水或添加胆维丁乳喂养14 d。2周后,酵母多糖组、胆维丁乳+酵母多糖组腹腔注射酵母多糖混悬液,对照组、胆维丁乳组腹腔注射等量0.9%氯化钠溶液,18 h后处死各组小鼠,分别进行HE染色,观察肾脏组织病变情况;Western blot技术检测炎症因子蛋白表达;用TRizol法按照试剂说明书提取总RNA,用反转录试剂盒将RNA反转录成c DNA;采用SPSS 16.0进行统计学处理。结果胆维丁乳+酵母多糖组小鼠炎症因子IL-6、IL-18蛋白及mRNA的表达、尿素及肌酐水平高于酵母多糖组(P<0.05),且肾脏组织病理学改变较严重。结论对于正常生长的小鼠,给予胆维丁乳不会加重小鼠的肾脏负担;对于已经发生急性肾损伤的小鼠,胆维丁乳的摄入会加重肾脏损伤。 | 孙灿 刘凯 赵晴 孔娟 | 2016 | 实用药物与临床2016，19，12： | 0 |
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