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1Relationship between intestinal microbiota and ulcerative colitis:Mechanisms and clinical application of probiotics and fecal microbiota transplantation显示文摘Ulcerative colitis(UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. however, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation(FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in thepathogenesis and treatment of UC.Zhao-hua Shen Chang-xin Zhu Yong-sheng Quan Zhen-yu Yang Shuai Wu Wei-wei Luo Bei Tan Xiao-yan Wang 2018World Journal of Gastroenterology2018,24,1:111
2Inflammatory bowel disease:Pathogenesis显示文摘Inflammatory bowel disease(IBD),including Crohn’s disease and ulcerative colitis,is characterized by chronic relapsing intestinal inflammation.It has been a worldwide health-care problem with a continually increasing incidence.It is thought that IBD results from an aberrant and continuing immune response to the microbes in the gut,catalyzed by the genetic susceptibility of the individual.Although the etiology of IBD remains largely unknown,it involves a complex interaction between the genetic,environmental or microbial factors and the immune responses.Of the four components of IBD pathogenesis,most rapid progress has been made in the genetic study of gut inflammation.The latest internationally collaborative studies have ascertained 163susceptibility gene loci for IBD.The genes implicated in childhood-onset and adult-onset IBD overlap,suggesting similar genetic predispositions.However,the fact that genetic factors account for only a portion of overall disease variance indicates that microbial and environmental factors may interact with genetic elements in the pathogenesis of IBD.Meanwhile,the adaptive immune response has been classically considered to play a major role in the pathogenesis of IBD,as new studies in immunology and genetics have clarified that the innate immune response maintains the same importance in inducing gut inflammation.Recent progress in understanding IBD pathogenesis sheds lights on relevant disease mechanisms,including the innate and adaptive immunity,and the interactions between genetic factors and microbial and environmental cues.In this review,we provide an update on the major advances that have occurred in above areas.Yi-Zhen Zhang Yong-Yu Li 2014World Journal of Gastroenterology2014,20,1:103
3Moxibustion treatment modulates the gut microbiota and immune function in a dextran sulphate sodium-induced colitis rat model显示文摘AIM To investigate the effect and mechanism of moxibustion in rats with ulcerative colitis.METHODS A rat colitis model was established by administering 4% dextran sulphate sodium solution. Seventy male rats were randomly divided into seven groups: Healthy controls(HC), ulcerative colitis model group(UC), UC with 7 d of moxibustion(UC-7), UC with 14 d of moxibustion(UC-14), UC with mesalazine gavage(UC-W), HC with 7 d of moxibustion(HC-7), HC with 14 d of moxibustion(HC-14). Moxibustion was applied to the bilateral Tianshu(ST25). Gut microbiome profiling was conducted by 16 S r RNA amplicon sequencing, and PCR and ELISA determined the expression of inflammatory cytokines in colon mucosa and serum, respectively. RESULTS Moxibustion treatment restored the colonic mucosa and decreased submucosal inflammatory cell infiltration in colitis rats. Rats treated with moxibustion and mesalazine had significantly lower levels of the dominant phyla Proteobacteria and the genera Saccharibacteria, Sphingomonas and Barnesiella than colitis rats, and they could restore the microbiome to levels similar to those observed in healthy rats. UC rats had reduced alpha diversity, which could be alleviated by moxibustion therapy, and UC-7 had a higher alpha diversity than UC-14. This finding suggests that short-term(7 d) but no longer term(14 d) moxibustion treatment may significantly affect the gut microbiome. The potential bacterial functions affected by moxibustion may be ascorbate and aldarate metabolism, and amino acid metabolism. Compared with HC group, the levels of the cytokines interleukin-12(IL-12)(P < 0.05) and IL-6, IL-17, IL-23, interferon-γ, lipopolysaccharide, Ig A, tumour necrosis factor-α and its receptors 1(TNFR1) and TNFR2(P < 0.01) were all increased, whereas anti-inflammatory cytokine IL-2 and IL-10(P < 0.01) and transforming growth factor-β(P < 0.05) were decreased in UC rats. These changes were reversed by moxibustion.CONCLUSION Our findings suggest that moxibustion exerts its therapeutic effect by repairing mucosal tissue damage and modulating the gut microbiome and intestinal mucosal immunity.Qin Qi Ya-Nan Liu Xiao-Ming Jin Lin-Shuang Zhang Cun Wang Chun-Hui Bao Hui-Rong Liu Huan-Gan Wu Xiao-Mei Wang 2018World Journal of Gastroenterology2018,24,28:42
4Epidemiology, demographic characteristics and prognostic predictors of ulcerative colitis显示文摘Ulcerative colitis(UC)is a chronic disease characterized by diffuse inflammation of the mucosa of the colon and rectum.The hallmark clinical symptom of UC is bloody diarrhea.The clinical course is marked by exacerbations and remissions,which may occur spontaneously or in response to treatment changes or intercurrent illnesses.UC is most commonly diagnosed in late adolescence or early adulthood,but it can occur at any age.The incidence of UC has increased worldwide over recent decades,especially in developing nations.In contrast,during this period,therapeutic advances have improved the life expectancy of patients,and there has been a decrease in the mortality rate over time.It is important to emphasize that there is considerable variability in the phenotypic presentation of UC.Within this context,certain clinical and demographic characteristics are useful in identifying patients who tend to have more severe evolution of the disease and a poor prognosis.In this group of patients,better clinical surveillance and more intensive therapy may change the natural course of the disease.The aim of this article was to review the epidemiology and demographic characteristics of UC and the factors that may be associated with its clinical prognosis.Bruno César da Silva Andre Castro Lyra Raquel Rocha Genoile Oliveira Santana 2014World Journal of Gastroenterology2014,20,28:48
5A chronic ulcerative colitis model in rats显示文摘INTRODUCTIONIn recent years,there have been many reports aboutanimal model to investigate drugs for inflammatorybowel diseases (IBD).The experimental animalmodel often used is acetic acid-induced damage ofcolonic muscosa.In the present study,this animalmodel was investigated by administering variousconcentrations of TNBS.Zheng L Gao ZQ Wang SX 2000World Journal of Gastroenterology2000,6,1:37
6Contribution 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 2015World Journal of Gastroenterology2015,21,19:37
7Ulcerative colitis-associated colorectal cancer显示文摘The association between ulcerative colitis(UC) and colorectal cancer(CRC) has been acknowledged. One of the most serious and life threatening consequences of UC is the development of CRC(UC-CRC). UC-CRC patients are younger, more frequently have multiple cancerous lesions, and histologically show mucinous or signet ring cell carcinomas. The risk of CRC begins to increase 8 or 10 years after the diagnosis of UC. Risk factors for CRC with UC patients include young age at diagnosis, longer duration, greater anatomical extent of colonic involvement, the degree of inflammation, family history of CRC, and presence of primary sclerosing cholangitis. CRC on the ground of UC develop from non-dysplastic mucosa to indefinite dysplasia, lowgrade dysplasia, high-grade dysplasia and finally to invasive adenocarcinoma. Colonoscopy surveillance programs are recommended to reduce the risk of CRC and mortality in UC. Genetic alterations might play a role in the development of UC-CRC. 5-aminosalicylates might represent a favorable therapeutic option for chemoprevention of CRC.Masakazu Yashiro 2014World Journal of Gastroenterology2014,20,44:39
8Tight junctions in inflammatory bowel diseases and inflammatory bowel disease associated colorectal cancer显示文摘Inflammatory bowel diseases are characterised by inflammation that compromises the integrity of the epithelial barrier. The intestinal epithelium is not only a static barrier but has evolved complex mechanisms to control and regulate bacterial interactions with the mucosal surface. Apical tight junction proteins are critical in the maintenance of epithelial barrier function and control of paracellular permeability. The characterisation of alterations in tight junction proteins as key players in epithelial barrier function in inflammatory bowel diseases is rapidly enhancing our understanding of critical mechanisms in disease pathogenesis as well as novel therapeutic opportunities. Here we give an overview of recent literature focusing on the role of tight junction proteins, in particular claudins, in inflammatory bowel diseases and inflammatory bowel disease associated colorectal cancer.Jonathan Landy Emma Ronde Nick English Sue K Clark Ailsa L Hart Stella C Knight Paul J Ciclitira Hafid Omar Al-Hassi 2016World Journal of Gastroenterology2016,22,11:39
9Implication of miRNAs for inflammatory bowel disease treatment:Systematic review显示文摘Inflammatory bowel disease(IBD)is believed to develop via a complex interaction between genetic,environmental factors and the mucosal immune system.Crohn’s disease and ulcerative colitis are two major clinical forms of IBD.MicroRNAs(miRNAs)are a class of small,endogenous,noncoding RNA molecules,and evolutionary conserved in animals and plants.It controls protein production at the post-transcriptional level by targeting mRNAs for translational repression or degradation.MiRNAs are important in many biological processes,such as signal transduction,cellular proliferation,differentiation and apoptosis.Considerable attention has been paid on the key role of miRNAs in autoimmune and inflammatory disease,especially IBD.Recent studies have identified altered miRNA profiles in ulcerative colitis,Crohn’s disease and inflammatory bowel diseaseassociated colorectal cancer.In addition,emerging data have implicated that special miRNAs which suppress functional targets play a critical role in regulating key pathogenic mechanism in IBD.MiRNAs were found involving in regulation of nuclear transcription factor kappa B pathway(e.g.,miR-146a,miR-146b,miR-122,miR-132,miR-126),intestinal epithelial barrier function(e.g.,miR-21,miR-150,miR-200b)and the autophagic activity(e.g.,miR-30c,miR-130a,miR-106b,miR-93,miR-196).This review aims at discussing recent advances in our understanding of miRNAs in IBD pathogenesis,their role as disease biomarkers,and perspective for future investigation and clinical application.Wei-Xu Chen Li-Hua Ren Rui-Hua Shi 2014World Journal of Gastrointestinal Pathophysiology2014,5,2:31
10Role of moxibustion in inflammatory responses during treatment of rat ulcerative colitis显示文摘AIM: To investigate the efficacy of moxibustion in ulcerative colitis(UC) rats from morphological, immunological and molecular biological perspectives.METHODS: Thirty-two Sprague-Dawley rats were randomly assigned to a blank control group(normal rats, n = 6) and a model replication(MR) group(UC rats, n = 26). A UC model was established by 2,4,6-trinitrobenzenesulfonic acid/dextran sulfate sodium enema. Rats in the MR group were further randomly assigned to a 9-min moxibustion(9M) group(9 moxa-cone, n = 6), 6-min moxibustion(6M) group(6 moxa-cone, n = 6), 3-min moxibustion(3M) group(3 moxa-cone, n = 6), and a waiting list control(WLC) group(no moxibustion treatment, n = 6). Rats in the moxibustion treatment group were treated in 14 sessions over 28 d. Disease activity, local tissue morphology, serum level of interleukin(IL)-8 and IL-10, and expression of Toll-like receptor(TLR)9 aswell as nuclear factor(NF)-κB p65 in colonic tissue were determined by disease activity index(DAI), hematoxylin and eosin staining, electron microscopy, enzyme-linked immunosorbent assay and Western blotting, respectively.RESULTS: DAI was lowest in the 9M group and highest in the WLC group. The differences in DAI between the moxibustion treatment(3M, 6M, 9M) and no treatment groups were significant for all one-to-one comparisons(0.60 ± 0.54 vs 1.20 ± 0.44, 0.60 ± 0.54 vs 1.80 ± 0.45, 0.60 ± 0.54 vs 3.0 ± 0.45, respectively, P < 0.05). Light and electron microscopy showed that the neatness of the glandular arrangement in colonic mucosal epithelia gradually increased in the WLC, 3M, 6M to 9M groups. IL-8 level successively decreased while IL-10 level increased from the WLC to 3M, 6M and 9M groups. The differences among these groups were significant for all comparisons(105.46 ± 8.75 vs 76.61 ± 3.58, 105.46 ± 8.75 vs 69.78 ± 1.87, 105.46 ± 8.75 vs 67.41 ± 1.84, respectively, P < 0.01 for IL-8; and 30.83 ± 1.29 vs 75.64 ± 1.90, 30.83 ± 1.29 vs 80.90 ± 3.16, 30.83 ± 1.29 vs 83.46 ± 2.37, respectively, P < 0.01 for IL-10), except comparison of 6M vs 9M. Expression of TLR9 and NF-κB p65 decreased in order: highest in the WLC group and lowest in the 9M group. In addition, the differences among the WLC, 3M, 6M and 9M groups were significant for all comparisons(0.492 ± 0.026 vs 0.380 ± 0.022, 0.492 ± 0.026 vs 0.355 ± 0.005, 0.492 ± 0.026 vs 0.327 ± 0.015, respectively, P < 0.05 for TLR9; and 0.436 ± 0.041 vs 0.326 ± 0.022, 0.436 ± 0.041 vs 0.293 ± 0.006, 0.436 ± 0.041 vs 0.265 ± 0.017, respectively, P < 0.05 for NF-κB p65).CONCLUSION: Moxibustion repairs damaged colonic mucosa, suppresses serum IL-8, activates serum IL-10 level, and decreases expression of TLR-9 and NF-κB p65 in UC rats.Yang Han Tie-Ming Ma Mao-Lin Lu Lu Ren Xian-De Ma Zeng-Hua Bai 2014World Journal of Gastroenterology2014,20,32:27
11Unconjugated bilirubin alleviates experimental ulcerative colitis by regulating intestinal barrier function and immune inflammation显示文摘BACKGROUND Unconjugated bilirubin(UCB) is generally considered toxic but has gained recent prominence for its anti-inflammatory properties. However, the effects of it on the interaction between intestinal flora and organisms and how it influences immune responses remain unresolved.AIM To investigate the role of UCB in intestinal barrier function and immune inflammation in mice with dextran-sulfate-sodium-induced colitis.METHODS Acute colitis was induced by 3%(w/v) dextran sulfate sodium salt in drinking water for 6 d followed by untreated water for 2 d. Concurrently, mice with colitis were administered 0.2 mL UCB(400 μmol/L) by intra-gastric gavage for 7 d.Disease activity index(DAI) was monitored daily. Mice were sacrificed at the end of the experiment. The length of the colon and weight of the spleen were recorded. Serum level of D-lactate, intestinal digestive proteases activity, and changes to the gut flora were analyzed. In addition, colonic specimens were analyzed by histology and for expression of inflammatory markers and proteins.RESULTS Mice treated with UCB had significantly relieved severity of colitis, including lower DAI, longer colon length, and lower spleen weight(colon length: 4.92 ±0.09 cm vs 3.9 ± 0.15 cm; spleen weight: 0.33 ± 0.04 vs 0.74 ± 0.04, P < 0.001). UCB administration inactivated digestive proteases(chymotrypsin: 18.70 ± 0.69 U/g vs44.81 ± 8.60 U/g; trypsin: 1.52 ± 0.23 U/g vs 9.05 ± 1.77 U/g, P < 0.01), increased expression of tight junction(0.99 ± 0.05 vs 0.57 ± 0.03, P < 0.001), decreased serum level of D-lactate(31.76 ± 3.37 μmol/L vs 54.25 ± 1.45 μmol/L, P < 0.001), and lowered histopathological score(4 ± 0.57 vs 7 ± 0.57, P < 0.001) and activity of myeloperoxidase(46.79 ± 2.57 U/g vs 110.32 ± 19.19 U/g, P < 0.001). UCB also regulated the intestinal microbiota, inhibited expression of tumor necrosis factor(TNF) α and interleukin 1β(TNF-α: 52.61 ± 7.81 pg/mg vs 105.04 ± 11.92 pg/mg,interleukin 1β: 13.43 ± 1.68 vs 32.41 ± 4.62 pg/mg, P < 0.001), decreased expression of Toll-like receptor 4(0.61 ± 0.09 vs 1.07 ± 0.03, P < 0.001) and myeloid differentiation primary response gene 88(0.73 ± 0.08 vs 1.01 ± 0.07, P <0.05), and increased expression of TNF-receptor-associated factor 6(0.79 ± 0.02 vs0.43 ± 0.09 P < 0.05) and inhibitor of kappa B α(0.93 ± 0.07 vs 0.72 ± 0.07, P < 0.05)in the colon.CONCLUSION UCB can protect intestinal barrier function, regulate normal intestinal homeostasis, and suppress inflammation via the Toll-like receptor 4/nuclear factor-κB signaling pathway.Jia-Dong Zheng Yan He Heng-Yuan Yu Yuan-Li Liu Yi-Xuan Ge Xue-Ting Li Xue Li Yan Wang Meng-Ru Guo Yi-Lin Qu Xiao-Fa Qin Ming-Shan Jiang Xiu-Hong Wang 2019World Journal of Gastroenterology2019,25,15:26
12Multicenter case-control study of the risk factors for ulcerative colitis in China显示文摘AIM:To evaluate potential risk factors in the development of ulcerative colitis(UC) in China.METHODS:A total of 1308 patients with UC and 1308 age-matched and sex-matched controls were prospectively studied in China.The UC cases were collected from 17 hospitals in China from April 2007 to April 2010.Uniform questionnaires were designed to investigate risk factors including smoking,appendectomy,stress,socio-economic conditions,nonsteroidal antiinflammatory drugs(NSAIDs),oral contraceptives,diet,breastfeeding,infections and family sanitary conditions.Group comparisons by each factor were done using simple logistic regression analysis.Conditional logistic regression was used for multivariate analysis.RESULTS:By univariate analysis,the variables predictive of UC included feeling stress,light and heavy alcoholic drinking,spicy food,sugar consumption and infectious diarrhea,while heavy tea intake and tap water consumption were protective against UC.On multivariate analysis,the protective factor for UC was tap water consumption [odds ratios(OR) = 0.424,95%CI:0.302-0.594,P < 0.001];while the potential risk factors for UC were heavy sugar consumption(OR = 1.632,95%CI:1.156-2.305,P < 0.001),spicy food(light intake:OR = 3.329,95%CI:2.282-4.857,P < 0.001;heavy intake:OR = 3.979,95%CI:2.700-5.863,P < 0.001),and often feeling stress(OR = 1.981,95%CI:1.447-2.711,P < 0.001).Other factors,such as smoking habit,appendectomy,breastfeeding,a history of measles,rural or urban residence,education,oral contraceptives,and NSAID use have not been found to have a significant association with the development of UC in the present study.CONCLUSION:Our study showed tap water consumption was a protective factor for UC,while spicy food,heavy sugar consumption and often feeling stress were risk factors for UC in this Chinese population.Yu-Fang Wang Qin Ou-yang Bing Xia Li-Na Liu Fang Gu Kai-Fang Zhou Qiao Mei Rui-Hua Shi Zhi-Hua Ran Xiao-Di Wang Pin-Jin Hu Kai-Chun Wu Xin-Guang Liu Ying-Lei Miao Ying Han Xiao-Ping Wu Guo-Bing He Jie Zhong Guan-Jian Liu 2013World Journal of Gastroenterology2013,19,11:24
13Effect of resveratrol on Treg/Th17 signaling and ulcerative colitis treatment in mice显示文摘AIM:To determine the therapeutic efficacy of resveratrol on ulcerative colitis(UC) and its underlying mechanisms.METHODS:The mouse UC model was developed using 5% dextran sulfate sodium.Mice were randomly divided into four groups:normal control,UC model group,resveratrol low-dose group(RLD; 50 mg/kg per day),and resveratrol high-dose group(RHD; 100 mg/kg per day).RESULTS:The results showed that RLD regulates Treg/Th17 balance mainly through reducing the number of Th17 cells,whereas RHD regulates Treg/Th17 balance through both downregulating the number of Th17 cells and upregulating the number of Treg cells.Resveratrol can also regulate the level of plasma and intestinal mucosal cytokines including interleukin(IL)-10,transforming growth factor-β1,IL-6,and IL-17.The expressions of hypoxia inducible factor(HIF)-1α,mammalian target of rapamycin(m TOR),and signal transducer and activator of transcription 3 weresignificantly decreased in the intestinal tissues of mice treated with resveratrol.CONCLUSION:The therapeutic efficacy of resveratrol in UC is dose dependent and closely associated with the regulation of Treg/Th17 balance and the HIF-1α/mT OR signaling pathway.Jun Yao Cheng Wei Jian-Yao Wang Ru Zhang Ying-Xue Li Li-Sheng Wang 2015World Journal of Gastroenterology2015,21,21:23
14Diet therapy for inflammatory bowel diseases: The established and the new显示文摘Although patients with inflammatory bowel diseases(IBD) have a strong interest in dietary modifications as part of their therapeutic management, dietary advice plays only a minor part in published guidelines. The scientific literature shows that dietary factors might influence the risk of developing IBD, that dysbiosis induced by nutrition contributes to the pathogenesis of IBD, and that diet may serve as a symptomatic treatment for irritable bowel syndrome-like symptoms in IBD. The role of nutrition in IBD is underscored by the effect of various dietary therapies. In paediatric patients with Crohn's disease(CD) enteral nutrition(EN) reaches remission rates similar to steroids. In adult patients, however, EN is inferior to corticosteroids. EN is not effective in ulcerative colitis(UC). Total parenteral nutrition in IBD is not superior to steroids or EN. The use of specific probiotics in patients with IBD can be recommended only in special clinical situations. There is no evidence for efficacy of probiotics in CD. By contrast, studies in UC have shown a beneficial effect in selected patients. For patients with pouchitis, antibiotic treatment followed by probiotics, like VSL#3 or Lactobacillus GG, is effective. When probiotics are used, the risk of bacterial translocation and subsequent bacteremia has to be considered. More understanding of the normal intestinal microflora, and better characterization of probiotic strains at the phenotypic and genomic levels is needed as well as clarification of the mechanisms of action in different clinical settings. A FODMAP reduced diet may improve symptoms in IBD.Franziska Durchschein Wolfgang Petritsch Heinz F Hammer 2016World Journal of Gastroenterology2016,22,7:22
15Endoscopy in inflammatory bowel disease: Role in diagnosis, management, and treatment显示文摘Endoscopy plays a fundamental role in the diagnosis, management, and treatment of inflammatory bowel dis-ease(IBD). Colonoscopy, flexible sigmoidoscopy, and esophagogastroduodenoscopy have long been used in the care of patients with IBD. As endoscopic technologies have progressed, tools such as endoscopic ultrasound, capsule endoscopy, and balloon-assisted enteroscopy have expanded the role of endoscopy in IBD. Furthermore, chromoendoscopy has enhanced our ability to detect dys-plasia in IBD. In this review article, we will focus on the roles, indications, and limitations of these tools in IBD. We will also discuss the most commonly used endoscopic scoring systems, as well as special considerations in post-surgical patients. Lastly, we will discuss the role of endoscopy in the diagnosis and management of fistulae and strictures.Clayton M Spiceland Nilesh Lodhia 2018World Journal of Gastroenterology2018,24,35:23
16Colorectal cancer surveillance in inflammatory bowel disease:Practice guidelines and recent developments显示文摘Patients with long-standing inflammatory bowel disease(IBD)involving at least 1/3 of the colon are at increased risk for colorectal cancer(CRC).Advancements in CRC screening and surveillance and improved treatment of IBD has reduced CRC incidence in patients with ulcerative colitis and Crohn’s colitis.Most cases of CRC are thought to arise from dysplasia,and recent evidence suggests that the majority of dysplastic lesions in patients with IBD are visible,in part thanks to advancements in high definition colonoscopy and chromoendoscopy.Recent practice guidelines have supported the use of chromoendoscopy with targeted biopsies of visible lesions rather than traditional random biopsies.Endoscopists are encouraged to endoscopically resect visible dysplasia and only recommend surgery when a complete resection is not possible.New technologies such as virtual chromoendoscopy are emerging as potential tools in CRC screening.Patients with IBD at increased risk for developing CRC should undergo surveillance colonoscopy using new approaches and techniques.William T Clarke Joseph D Feuerstein 2019World Journal of Gastroenterology2019,25,30:23
17Progress in active compounds effective on ulcerative colitis from Chinese medicines显示文摘Ulcerative colitis(UC), a chronic inflammatory disease affecting the colon, has a rising incidence worldwide. The known pathogenesis is multifactorial and involves genetic predisposition, epithelial barrier defects, dysregulated immune responses, and environmental factors. Nowadays, the drugs for UC include 5-aminosalicylic acid, steroids, and immunosuppressants. Long-term use of these drugs, however, may cause several side effects, such as hepatic and renal toxicity, drug resistance and allergic reactions. Moreover, the use of traditional Chinese medicine(TCM) in the treatment of UC shows significantly positive effects, low recurrence rate, few side effects and other obvious advantages. This paper summarizes several kinds of active compounds used in the experimental research of anti-UC effects extracted from TCM, mainly including flavonoids, acids, terpenoids, phenols, alkaloids, quinones, and bile acids from some animal medicines. It is found that the anti-UC activities are mainly focused on targeting inflammation or oxidative stress, which is associated with increasing the levels of anti-inflammatory cytokine(IL-4, IL-10, SOD), suppressing the levels of pro-inflammatory cytokines(TNF-α, IL-1β, IL-6, IL-8, IL-23, NF-κB, NO), reducing the activity of MPO, MDA, IFN-γ, and iNOS. This review may offer valuable reference for UC-related studies on the compounds from natural medicines.CAO Si-Yu YE Sheng-Jie WANG Wei-Wei WANG Bing ZHANG Tong PU Yi-Qiong 2019Chinese Journal of Natural Medicines2019,17,2:23
18Inflammatory colonic carcinogenesis: A review on pathogenesis and immunosurveillance mechanisms in ulcerative colitis显示文摘Ulcerative colitis(UC)is characterized by repeated flare-ups of inflammation that can lead to oncogenic insults to the colonic epithelial.UC-associated carcinogenesis presents a different sequence of tumorigenic events compared to those that contribute to the development of sporadic colorectal cancer.In fact,in UC,the early events are represented by oxidative DNA damage and DNA methylation that can produce an inhibition of oncosuppressor genes,mutation of p53,aneuploidy,and microsatellite instability.Hypermethylation of tumor suppressor and DNA mismatch repair gene promoter regions is an epigenetic mechanism of gene silencing that contribute to tumorigenesis and may represent the first step in inflammatory carcinogenesis.Moreover,p53 is frequently mutated in the early stages of UC-associated cancer.Aneuploidy is an independentrisk factor for forthcoming carcinogenesis in UC.Epithelial cell-T-cell cross-talk mediated by CD80 is a key factor in controlling the progression from low to high grade dysplasia in UC-associated carcinogenesis.Marco Scarpa Ignazio Castagliuolo Carlo Castoro Anna Pozza Melania Scarpa Andromachi Kotsafti Imerio Angriman 2014World Journal of Gastroenterology2014,20,22:22
19Effectiveness of probiotic therapy for the prevention of relapse in patients with inactive ulcerative colitis显示文摘AIM: to evaluate the effectiveness of probiotic therapy for suppressing relapse in patients with inactive ulcerative colitis(UC).METHODS: Bio-Three tablets, each containing 2 mg of lactomin(Streptococcus faecalis T-110), 10 mg of Clostridium butyricum TO-A, and 10 mg of Bacillus mesentericus TO-A, were used as probiotic therapy.Sixty outpatients with UC in remission were randomly assigned to receive 9 Bio-Three tablets/day(BioThree group) or 9 placebo tablets/day(placebo group)for 12 mo in addition to their ongoing medications.Clinical symptoms were evaluated monthly or on the exacerbation of symptoms or need for additional medication. Fecal samples were collected to analyze bacterial DNA at baseline and 3-mo intervals. Terminal restriction fragment length polymorphism and cluster analyses were done to examine bacterial components of the fecal microflora.RESULTS: Forty-six patients, 23 in each group,completed the study, and 14 were excluded. The relapse rates in the Bio-Three and placebo groups were respectively 0.0% vs 17.4% at 3 mo(P = 0.036), 8.7%vs 26.1% at 6 mo(P = 0.119), and 21.7% vs 34.8%(P = 0.326) at 9 mo. At 12 mo, the remission rate was 69.5% in the Bio-Three group and 56.6% in the placebo group(P = 0.248). On cluster analysis of fecal flora, 7 patients belonged to cluster Ⅰ, 32 to cluster Ⅱ,and 7 to cluster Ⅲ.CONCLUSION: Probiotics may be effective formaintaining clinical remission in patients with quiescent UC, especially those who belong to cluster Ⅰ on fecal bacterial analysis.Yasushi Yoshimatsu Akihiro Yamada Ryuichi Furukawa Koji Sono Aisaku Osamura Kentaro Nakamura Hiroshi Aoki Yukiko Tsuda Nobuo Hosoe Nobuo Takada Yasuo Suzuki 2015World Journal of Gastroenterology2015,21,19:21
20Fluctuations in butyrate-producing bacteria in ulcerative colitis patients of North India显示文摘AIM: To study the interplay between butyrate concentration and butyrate-producing bacteria in fecal samples of ulcerative colitis (UC) patients vs control individuals. METHODS: Fecal samples were collected from 14 control individuals (hemorrhoid patients only) and 26 UC patients (severe: n = 12, moderate: n = 6, remission: n = 8), recruited by the gastroenterologist at the Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, India. Disease activity in UC patients was determined by clinical colitis activity index. We employed fluorescent in situ hybridization in combination with flow cytometry to enumerate the clostridium cluster population targeted by 16S rRNA gene probe. Major butyrate-producing species within this cluster were quantified to see if any change existed in control vs UC patients with different disease activity. This observed change was further validated by quantitative polymerase chain reaction. In addition to this,we carried out gas chromatography to evaluate the changes in concentration of major short chain fatty acids (SCFAs), namely acetate, n -butyrate, iso -butyrate, in the above samples. Student t test and Graph pad prism-6 were used to compare the data statistically. RESULTS: There was a significant decrease of Clostridium coccoides (control, 25.69% ± 1.62% vs severe, 9.8% ± 2.4%, P = 0.0001) and Clostridium leptum clusters (control, 13.74% ± 1.05% vs severe, 6.2% ± 1.8%, P = 0.0001) in fecal samples of UC patients. Furthermore, we demonstrated that some butyrateproducing members of the clostridial cluster, like Fecalibacterium prausnitzii (control, 11.66% ± 1.55% vs severe, 6.01% ± 1.6%, P = 0.0001) and Roseburia intestinalis (control, 14.48% ± 1.52% vs severe, 9% ± 1.83%, P = 0.02) were differentially present in patients with different disease activity. In addition, we also demonstrated decreased concentrations of fecal SCFAs, especially of n -butyrate (control, 24.32 ± 1.86 mmol/μL vs severe, 12.74 ± 2.75 mmol/μL, P = 0.003), iso -butyrate (control, 1.70 ± 0.41 mmol/μL vs severe, 0.68 ± 0.24 mmol/μL, P = 0.0441) and acetate (control, 39.51 ± 1.76 mmol/μL vs severe, 32.12 ± 2.95 mmol/ μL,P = 0.047), in the fecal samples of UC patients. The observed decrease of predominant butyrate producers of clostridial clusters correlated with the reduced SCFA levels in active UC patients. This was further confirmed by the restoration in the population of some butyrate producers with simultaneous increase in the level of SCFA in remission samples. CONCLUSION: Our observations indicate that decreases in members of the clostridial cluster resulting in reduced butyrate levels contribute to the etiology of UC.Reena Kumari Vineet Ahuja Jaishree Paul 2013World Journal of Gastroenterology2013,19,22:21
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