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| 1 | Relationship 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 | 2018 | World Journal of Gastroenterology2018，24，1： | 111 |
| 2 | Fecal microbiota transplantation broadening its application beyond intestinal disorders显示文摘Intestinal dysbiosis is now known to be a complication in a myriad of diseases.Fecal microbiota transplantation(FMT),as a microbiota-target therapy,is arguably very effective for curing Clostridium difficile infection and has good outcomes in other intestinal diseases.New insights have raised an interest in FMT for the management of extra-intestinal disorders associated with gut microbiota.This review shows that it is an exciting time in the burgeoning science of FMT application in previously unexpected areas,including metabolic diseases,neuropsychiatric disorders,autoimmune diseases,allergic disorders,and tumors.A randomized controlled trial was conducted on FMT in metabolic syndrome by infusing microbiota from lean donors or from self-collected feces,with the resultant findings showing that the lean donor feces group displayed increased insulin sensitivity,along with increased levels of butyrate-producing intestinal microbiota.Case reports of FMT have also shown favorable outcomes in Parkinson's disease,multiple sclerosis,myoclonus dystonia,chronic fatigue syndrome,and idiopathic thrombocytopenic purpura.FMT is a promising approach in the manipulation of the intestinal microbiota and has potential applications in a variety of extra-intestinal conditions associated with intestinal dysbiosis. | Meng-Que Xu Hai-Long Cao Wei-Qiang Wang Shan Wang Xiao-Cang Cao Fang Yan Bang-Mao Wang | 2015 | World Journal of Gastroenterology2015，21，1： | 63 |
| 3 | Relationship between plasma D(-)-lactate and intestinal damage after severe injuries in rats显示文摘AIM To explore the kinetic changes in plasma D (-)lactate and lipopolysaccharide ( LPS ) levels, and investigate whether D (-)-lactate could be used as a marker of intestinal injury in rats following gut ischemia/reperfusion, burn, and acute necrotizing pancreatitis (ANP).METHODS Three models were developed in rats:gut ischemia/reperfusion obtained by one hour of superior severe burn injury created by 30% of total body surface induced by continuous inverse infusion of sodium taurocholate and trypsin into main pancreatic duct.Plasma levels of D( - )-lactate in systemic circulation and LPS in portal circulation were measured by enzymaticspectrophotometric method and limulus amebocyte lysate (LAL) test kit, respectively. Tissue samples of intestine were taken for histological analysis.RESULTS One hour gut ischemia followed by reperfusion injuries resulted in a significant elevation in plasma D( - )lactate and LPS levels, and there was a significant correlation between the plasma D( - )-lactate and LPS (r =0.719, P<0.05). The plasma concentrations of D(-)lactate and LPS increased significantly at 6 h postburn,and there was also a remarkable correlation between them (r = 0.877, P < 0.01). D ( - )-lactate and LPS levels elevated significantly at 2 h after ANP, with a similar significant correlation between the two levels (r-0.798,P < 0.01 ). The desquamation of intestine villi and infiltration of inflammatory cells in the lamina propria were observed in all groups.CONCLUSION The changes of plasma D( - )-lactate levels in systemic blood paralleled with LPS levels in the portal vein blood. The measurement of plasma D (-)-lactate level may be a useful marker to assess the intestinal injury and to monitor an increase of intestinal permeability and endotoxemia following severe injuries in early stage. | Xiao-Qing Sun Xiao-Bing Fu Rong-Zhan Yi Lü Qun Deng Xiao-Guo Jian Zhi-Yong Sheng Bum Institute, 304~(th)Hospital,Beijing 100037,China Department of General Surgery,Chinese PLA 304 Hospital,Beijing 100037,China | 2001 | World Journal of Gastroenterology2001，7，4： | 56 |
| 4 | Effects of different resuscitation fluid on severe acute pancreatitis显示文摘AIM: To compare effects of different resuscitation fluid on microcirculation, inflammation, intestinal barrier and clinical results in severe acute pancreatitis (SAP). METHODS: One hundred and twenty patients with SAP were enrolled at the Pancreatic Disease Institute between January 2007 and March 2010. The patients were randomly treated with normal saline (NS group), combination of normal saline and hydroxyethyl starch (HES) (SH group), combination of normal saline, hydroxyethyl starch and glutamine (SHG group) in resuscitation. The ratio of normal saline to HES in the SH and SHG groups was 3:1. The glutamine (20% glutamine dipeptide, 100 mL/d) was supplemented into the resuscitation liquid in the SHG group. Complications and outcomes including respiratory and abdominal infection, sepsis, abdominal hemorrhage, intra-abdominal hypertension, abdominal compartment syndrome (ACS), renal failure, acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome (MODS), operation intervention, length of intensive care unit stay, length of hospital stay, and mortality at 60 d were compared. Moreover, blood oxygen saturation (SpO 2 ), gastric intramucosal pH value (pHi), intra-abdominal pressure (IAP), inflammation cytokines, urine lactulose/mannitol (L/M) ratio, and serum endotoxin were investigated to evaluate the inflammatory reaction and gut barrier. RESULTS: Compared to the NS group, patients in the SH and SHG groups accessed the endpoint more quickly (3.9 ± 0.23 d and 4.1 ± 0.21 d vs 5.8 ± 0.25 d, P < 0.05) with less fluid volume (67.26 ± 28.53 mL/kg/d, 61.79 ± 27.61 mL/kg per day vs 85.23 ± 21.27 mL/kg per day, P < 0.05). Compared to the NS group, incidence of renal dysfunction, ARDS, MODS and ACS in the SH and SHG groups was obviously lower. Furthermore, incidence of respiratory and abdominal infection was significantly decreased in the SH and SHG groups, while no significant difference in sepsis was seen. Moreover, less operation time was needed in the SH and SHG group than the NS group, but the difference was not significant. The mortality did not differ significantly among these groups. Blood SpO 2 and gastric mucosal pHi in the SH and SHG groups increased more quickly than in the NS group, while IAP was significantly decreased in the SH and SHG group. Moreover, the serum tumor necrosis factor-α, interleukin-8 and C-reactive protein levels in the SH and SHG groups were obviously lower than in the NS group at each time point. Furthermore, urine L/M ratio and serum endotoxin were significantly lower in the SH group and further decreased in the SHG group.CONCLUSION: Results indicated that combination of normal saline, HES and glutamine are more efficient in resuscitation of SAP by relieving inflammation and sustaining the intestinal barrier. | Gang Zhao Jun-Gang Zhang He-Shui Wu Jin Tao Qi Qin Shi-Chang Deng Yang Liu Lin Liu Bo Wang Kui Tian Xiang Li Shuai Zhu Chun-You Wang | 2013 | World Journal of Gastroenterology2013，19，13： | 56 |
| 5 | Increased numbers of Foxp3-positive regulatory T cells in gastritis, peptic ulcer and gastric adenocarcinoma显示文摘AIM: To determine the number of regulatory T cells (Tregs) in gastric mucosa of patients with gastritis, peptic ulcers and gastric cancer. METHODS: This study was a retrospective analysis of gastric antrum biopsy specimens from healthy controls (n = 22) and patients with gastritis (n = 30), peptic ulcer (n = 83), or gastric cancer (n = 32). Expression of CD4, CD25 and Foxp3 was determined by immunohistochemistry in three consecutive sections per sample.RESULTS: Compared with healthy controls, there was an increased number of CD25+ and Foxp3+ cells in patients with gastritis (P = 0.004 and P = 0.008), peptic ulcer (P < 0.001 and P < 0.001), and gastric cancer (P < 0.001 and P < 0.001). The ratio of CD25+/CD4+ or Foxp3+/CD4+ cells was also significantly higher in all disease groups (P < 0.001, respectively). The number of CD4+, CD25+, and Foxp3+ cells, and the ratio of CD25+/CD4+ and Foxp3+/CD4+ cells, were associated with the histological grade of the specimens, including acute inflammation, chronic inflammation, lymphoid follicle number, and Helicobacter pylori infection. The number of CD4+, CD25+ and Foxp3+ cells, and the ratio of CD25+/CD4+ and Foxp3+/CD4+ cells, were negatively associated with intestinal metaplasia among gastritis (P < 0.001, P < 0.001, P < 0.001, P = 0.002 and P = 0.002) and peptic ulcer groups (P = 0.013, P = 0.004, P < 0.001, P = 0.040 and P = 0.003). | Hsin-Hung Cheng Guan-Ying Tseng Hsiao-Bai Yang Hung-Jung Wang Hwai-Jeng Lin Wen-Ching Wang | 2012 | World Journal of Gastroenterology2012，18，1： | 56 |
| 6 | Treatment of Helicobacter pylori infection in atrophic gastritis显示文摘Helicobacter pylori(Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis(AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows:(1) Cure of infection, resolution of inflammation and normalization of gastric functions;(2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and(3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric p H, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroupof patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG. | Edith Lahner Marilia Carabotti Bruno Annibale | 2018 | World Journal of Gastroenterology2018，24，22： | 57 |
| 7 | Helicobacter pylori associated chronic gastritis,clinical syndromes,precancerous lesions,and pathogenesis of gastric cancer development显示文摘Helicobacter pylori(H.pylori)infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis(AG),or gastric intestinal metaplasia(GIM),and cancer.Various molecular alterations are identified not only in gastric cancer(GC)but also in precancerous lesions.H.pylori treatment seems to improve AG and GIM,but still remains controversial.In contrast,many studies,including meta-analysis,show that H.pylori eradication reduces GC.Molecular markers detected by genetic and epigenetic alterations related to carcinogenesis reverse following H.pylori eradication.This indicates that these changes may be an important factor in the identification of high risk patients for cancer development.Patients who underwent endoscopic treatment of GC are at high risk for development of metachronous GC.A randomized controlled trial from Japan concluded that prophylactic eradication of H.pylori after endoscopic resection should be used to prevent the development of metachronous GC,but recent retrospective studies did not show the tendency.Patients with precancerous lesions(molecular alterations)that do not reverse after H.pylori treatment,represent the'point of no return'and may be at high risk for the development of GC.Therefore,earlier H.pylori eradication should be considered for preventing GC development prior to the appearance of precancerous lesions. | Jiro Watari Nancy Chen Peter S Amenta Hirokazu Fukui Tadayuki Oshima Toshihiko Tomita Hiroto Miwa Kheng-Jim Lim Kiron M Das | 2014 | World Journal of Gastroenterology2014，20，18： | 60 |
| 8 | Gut-liver axis and probiotics: Their role in non-alcoholic fatty liver disease显示文摘The incidence of obesity and its related conditions, including non-alcoholic fatty liver disease(NAFLD), has dramatically increased in all age groups worldwide. Given the health consequences of these conditions, and the subsequent economic burden on healthcare systems, their prevention and treatment have become major priorities. Because standard dietary and lifestyle changes and pathogenically-oriented therapies(e.g., antioxidants, oral hypoglycemic agents, and lipid-lowering agents) often fail due to poor compliance and/or lack of efficacy, novel approaches directed toward other pathomechanisms are needed. Here we present several lines of evidence indicating that, by increasing energy extraction in some dysbiosis conditions or small intestinal bacterial overgrowth,specific gut microbiota and/or a'low bacterial richness'may play a role in obesity,metabolic syndrome,and fatty liver.Under conditions involving a damaged intestinal barrier('leaky gut'),the gut-liver axis may enhance the natural interactions between intestinal bacteria/bacterial products and hepatic receptors(e.g.,toll-like receptors),thus promoting the following cascade of events:oxidative stress,insulinresistance,hepatic inflammation,and fibrosis.We also discuss the possible modulation of gut microbiota by probiotics,as attempted in NAFLD animal model studies and in several pilot pediatric and adult human studies.Globally,this approach appears to be a promising and innovative add-on therapeutic tool for NAFLD in the context of multi-target therapy. | Giulia Paolella Claudia Mandato Luca Pierri Marco Poeta Martina Di Stasi Pietro Vajro | 2014 | World Journal of Gastroenterology2014，20，42： | 55 |
| 9 | Effect of mild moxibustion on intestinal microbiota and NLRP6 inflammasome signaling in rats with post-inflammatory irritable bowel syndrome显示文摘BACKGROUND About one-third of refractory irritable bowel syndrome(IBS)cases are caused by gastrointestinal(GI)infection/inflammation,known as post-infectious/postinflammatory IBS(PI-IBS).Although it is known that intestinal microbiota and host NOD-like receptor family pyrin domain containing 6(NLRP6)inflammsome signaling are closely related to PI-IBS and moxibustion has a therapeutic effect on PI-IBS,whether moxibustion regulates the intestinal flora and host NLRP6 events in PI-IBS remains unclear.AIM To examine the regulatory effect of moxibustion on intestinal microbiota and host NLRP6 inflammatory signaling in PI-IBS.METHODS Sprague-Dawley rats were divided into a normal control group,a model control group,a mild moxibustion group,and a sham mild moxibustion group.PI-IBS rats in the mild moxibustion group were treated with moxibusiton at bilateral Tianshu(ST 25)and Zusanli(ST36)for 7 consecutive days for 10 min each time.The sham group rats were given the same treatment as the mild moxibustion group except the moxa stick was not ignited.Abdominal withdrawal reflex(AWR)score was measured to assess the visceral sensitivity,and colon histopathology and ultrastructure,colonic myeloperoxidase(MPO)activity,and serum C-reactive protein(CRP)level were measured to evaluate low-grade colonic inflammation in rats.The relative abundance of selected intestinal bacteria in rat feces was detected by 16S rDNA PCR and the NLRP6 inflammsome signaling in the colon was detected by immunofluorescence,qRTPCR,and Western blot.RESULTS The AWR score was significantly decreased and the low-grade intestinal inflammation reflected by serum CRP and colonic MPO levels was inhibited in the mild moxibustion group compared with the sham group.Mild moxibustion remarkably increased the relative DNA abundances of Lactobacillus,Bifidobacterium,and Faecalibacterium prausnitzii but decreased that of Escherichia coli in the gut of PI-IBS rats.Additionally,mild moxibustion induced mRNA and protein expression of intestine lectin 1 but inhibited the expression of IL-1β,IL-18,and resistance-like moleculeβby promoting the NLRP6 and reducing the mRNA and protein expression of apoptosis-associated speck-like protein containing CARD(ASC)and cysteinyl-aspartate-specific proteinase 1(Caspase-1).The relative DNA abundances of Lactobacillus,Bifidobacteria,Faecalibacterium prausnitzii,and Escherichia coli in each group were correlated with the mRNA and protein expression of NLRP6,ASC,and Caspase-1 in the colon.CONCLUSION These findings indicated that mild moxibustion can relieve low-grade GI inflammation and alleviate visceral hypersensitivity in PI-IBS by regulating intestinal microbes and controlling NLRP6 inflammasome signaling. | Chun-Hui Bao Chun-Ye Wang Guo-Na Li Yi-Lu Yan Di Wang Xiao-Ming Jin Lu-Yi Wu Hui-Rong Liu Xiao-Mei Wang Zheng Shi Huan-Gan Wu | 2019 | World Journal of Gastroenterology2019，25，32： | 45 |
| 10 | Therapeutic effect of Qingyi decoction in severe acute pancreatitis-induced intestinal barrier injury显示文摘AIM: To investigate the effect of Qingyi decoction onthe expression of secreted phospholipase A2(s PLA2) in intestinal barrier injury.METHODS: Fifty healthy Sprague-Dawley rats were randomly divided into control, severe acute pancreatitis(SAP), Qingyi decoction-treated(QYT), dexamethasonetreated(DEX), and verapamil-treated(VER) groups. The SAP model was induced by retrograde infusion of 1.5% sodium deoxycholate into the biliopancreatic duct of the rats. All rats were sacrificed 24 h post-SAP induction. Arterial blood, intestine, and pancreas from each rat were harvested for investigations. The levels of serum amylase(AMY) and diamine oxidase(DAO) were determined using biochemical methods, and serum tumor necrosis factor(TNF)-α level was measured by an enzyme linked immunosorbent assay. Pathologic changes in the harvested tissues were investigated by microscopic examination of hematoxylin and eosinstained tissue sections. The expressions of s PLA2 at m RNA and protein levels were detected by reverse transcriptase PCR and Western blot, respectively. A terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling assay was used to investigate apoptosis of epithelial cells in the intestinal tissues. RESULTS: Compared to the control group, the expression of s PLA2 at both the m RNA and protein levels increased significantly in the SAP group(0.36 ± 0.13 vs 0.90 ± 0.38, and 0.16 ± 0.05 vs 0.64 ± 0.05, respectively; P s < 0.01). The levels of AMY, TNF-α and DAO in serum were also significantly increased(917 ± 62 U/L vs 6870 ± 810 U/L, 59.7 ± 14.3 ng/L vs 180.5 ± 20.1 ng/L, and 10.37 ± 2.44 U/L vs 37.89 ± 5.86 U/L, respectively; P s < 0.01). The apoptosis index of intestinal epithelial cells also differed significantly between the SAP and control rats(0.05 ± 0.02 vs 0.26 ± 0.06; P < 0.01). The serum levels of DAO and TNF-α, and the intestinal apoptosis index significantly correlated with s PLA2 expression in the intestine(r = 0.895, 0.893 and 0.926, respectively; Ps < 0.05). Thelevels of s PLA2, AMY, TNF-α, and DAO in the QYT, VER, and DEX groups were all decreased compared with the SAP group, but not the control group. Qingyi decoction intervention, however, gave the most therapeutic effect against intestinal barrier damage, although the onset of its therapeutic effect was slower. CONCLUSION: Qingyi decoction ameliorates acute pancreatitis-induced intestinal barrier injury by inhibiting the overexpression of intestinal s PLA2. This mechanism may be similar to that of verapamil. | Jing-Wen Zhang Gui-Xin Zhang Hai-Long Chen Ge-Liang Liu Lawrence Owusu Yu-Xi Wang Guan-Yu Wang Cai-Ming Xu | 2015 | World Journal of Gastroenterology2015，21，12： | 35 |
| 11 | Changes of plasma D(-) -lactate, diamine oxidase and endotoxin in patients with liver cirrhosis显示文摘BACKGROUND: Plasma D(-)-lactate and diamine oxidase (DAO) can reflect patients’ intestinal mucosal condition. We evaluated the changes of plasma D (-)-lactate, DAO and endotoxin activities and their significance in patients with liver cirrhosis. METHODS: Fifty liver cirrhosis patients were enrolled into experimental group and 30 healthy people into control group. The plasma levels of D(-)-lactate, DAO and endo- toxin were detected spectrophotographically. RESULTS: The level of D(-)-lactate was significantly high- er in the experimental group than that in the control group (P<0.01). Significant differences of D (-)-lactate levels were observed in Child-Pugh subgroups of the experimen- tal group (P <0. 01). The level of DAO was significantly higher in the experimental group than that in the control group (P <0.01), but the level of DAO in Child-Pugh sub- group C was significantly lower than that in Child-Pugh subgroup B (P<0.01). The level of endotoxin was signifi- cantly increased in the experimental group except Child Pugh subgroup A (P<0.01). The plasma levels of D(-) lactate, DAO and endotoxin were positively correlated with each other (P<0.01). CONCLUSIONS: The data suggest that both plasma D(-) lactate and DAO activity are sensitive markers for early diagnosis of gut failure and endotoxemia in patients with liver cirrhosis. The impairment of intestinal barrier func- tion may be one of the critical reasons for deterioration of liver cirrhosis. | Peng Ruan, Zuo-Jiong Gong and Quan-Rong Zhang Wuhan, China Department of Infectious Diseases, Renmin Hospital Wuhan University Medical College, Wuhan 430060 , China | 2004 | Hepatobiliary & Pancreatic Diseases International2004，3，1： | 31 |
| 12 | Challenges in diagnosing mesenteric ischemia显示文摘Early identification of acute mesenteric ischemia (AMI) is challenging. The wide variability in clinical presentation challenges providers to make an early accurate diagnosis. Despite major diagnostic and treatment advances over the past decades, mortality remains high. Arterial embolus and superior mesenteric artery thrombosis are common causes of AMI. Non-occlusive causes are less common, but vasculitis may be important, especially in younger people. Because of the unclear clinical presentation and non-specific laboratory findings, low clinical suspicion may lead to loss of valuable time. During this diagnostic delay, progression of ischemia to transmural bowel infarction with peritonitis and septicemia may further worsen patient outcomes. Several diagnostic modalities are used to assess possible AMI. Multi-detector row computed tomographic angiography is the current gold standard. Although computed tomographic angiography leads to an accurate diagnosis in many cases, early detection is a persistent problem. Because early diagnosis is vital to commence treatment, new diagnostic strategies are needed. A non-invasive simple biochemical test would be ideal to increase clinical suspicion of AMI and would improve patient selection for radiographic evaluation. Thus, AMI could be diagnosed earlier with follow-up computed tomographic angiography or high spatial magnetic resonance imaging. Experimental in vitro and in vivo studies show promise for alpha glutathione S transferase and intestinal fatty acid binding protein as markers for AMI. Future research must confirm the clinical utility of these biochemical markers in the diagnosis of mesenteric ischemia. | Teun C van den Heijkant Bart AC Aerts Joep A Teijink Wim A Buurman Misha DP Luyer | 2013 | World Journal of Gastroenterology2013，19，9： | 31 |
| 13 | Gut-liver axis in liver cirrhosis: How to manage leaky gut and endotoxemia显示文摘A 'leaky gut' may be the cutting edge for the passage of toxins, antigens or bacteria into the body, and may play a pathogenic role in advanced liver cirrhosis and its complications. Plasma endotoxin levels have been admitted as a surrogate marker of bacterial translocation and close relations of endotoxemia to hyperdynamic circulation, portal hypertension, renal, cardiac, pulmonary and coagulation disturbances have been reported. Bacterial overgrowth, increased intestinal permeability, failure to inactivate endotoxin,activated innate immunity are all likely to play a role in the pathological states of bacterial translocation. Therapeutic approach by management of the gut-liver axis by antibiotics, probiotics, synbiotics, prebiotics and their combinations may improve the clinical course of cirrhotic patients. Special concern should be paid on anti-endotoxin treatment. Adequate management of the gut-liver axis may be effective for prevention of liver cirrhosis itself by inhibiting the progression of fibrosis. | Hiroshi Fukui | 2015 | World Journal of Hepatology2015，7，3： | 32 |
| 14 | Intestinal barrier in inflammatory bowel disease显示文摘A complex mucosal barrier protects as the first line of defense the surface of the healthy intestinal tract from adhesion and invasion by luminal microorganisms.In this review,we provide an overview about the major components of this protective system as for example an intact epithelium,the synthesis of various antimicrobial peptides(AMPs)and the formation of the mucus layer.We highlight the crucial importance of their correct functioning for the maintenance of a proper intestinal function and the prevention of dysbiosis and disease.Barrier disturbances including a defective production of AMPs,alterations in thickness or composition of the intestinal mucus layer,alterations of pattern-recognition receptors,defects in the process of autophagy as well as unresolved endoplasmic reticulum stress result in an inadequate host protection and are thought to play a crucial role in the pathogenesis of the inflammatory bowel diseases Crohn’s disease and ulcerative colitis. | Lena Antoni Sabine Nuding Jan Wehkamp Eduard F Stange | 2014 | World Journal of Gastroenterology2014，20，5： | 33 |
| 15 | Intestinal microbiota in health and disease: Role of bifidobacteria in gut homeostasis显示文摘The pool of microbes inhabiting our body is known as 'microbiota' and their collective genomes as 'microbiome'. The colon is the most densely populated organ in the human body, although other parts, such as the skin, vaginal mucosa, or respiratory tract, also harbour specific microbiota. This microbial community regulates some important metabolic and physiological functions of the host, and drives the maturation of the immune system in early life, contributing to its homeostasis during life. Alterations of the intestinal microbiota can occur by changes in composition(dysbiosis), function, or microbiota-host interactions and they can be directly correlated with several diseases. The only disease in which a clear causal role of a dysbiotic microbiota has been demonstrated is the case of Clostridium difficile infections. Nonetheless, alterations in composition and function of the microbiota have been associated with several gastrointestinal diseases(inflammatory bowel disease, colorectal cancer, or irritable bowel syndrome), as well as extra-intestinal pathologies, such as those affecting the liver, or the respiratory tract(e.g., allergy, bronchial asthma, and cystic fibrosis), among others. Species of Bifidobacterium genus are the normal inhabitants of a healthy human gut and alterations in number and composition of their populations is one of the most frequent features present in these diseases. The use of probiotics, including bifidobacteria strains, in preventive medicine to maintain a healthy intestinal function is well documented. Probiotics are also proposed as therapeutic agents for gastrointestinal disorders and other pathologies. The World Gastroenterology Organization recently published potential clinical applications for several probiotic formulations, in which species of lactobacilli are predominant. This review is focused on probiotic preparations containing Bifidobacterium strains, alone or in combination with other bacteria, which have been tested in human clinical studies. In spite of extensive literature on and research into this topic, the degree of scientific evidence of the effectiveness of probiotics is still insufficient in most cases. More effort need to be made to design and conduct accurate human studies demonstrating the efficacy of probiotics in the prevention, alleviation, or treatment of different pathologies. | Rafael Tojo Adolfo Suárez Marta G Clemente Clara G de los Reyes-Gavilán Abelardo Margolles Miguel Gueimonde Patricia Ruas-Madiedo | 2014 | World Journal of Gastroenterology2014，20，41： | 33 |
| 16 | Protective effect of glutamine on intestinal injury and bacterial community in rats exposed to hypobaric hypoxia environment显示文摘AIM:To investigate the protective effect of glutamine(Gln)on intestinal injury and the bacterial community in rats exposed to hypobaric hypoxia environment.METHODS:Sprague-Dawley rats were divided into control,hypobaric hypoxia(HH),and hypobaric hypoxia+Gln(5.0 g/kg BW·d)(HG)groups.On the first 3 d,all rats were placed in a normal environment.After the third day,the HH and HG groups were transferred into a hypobaric chamber at a simulated elevation of 7000m for 5 d.The rats in the HG group were given Gln by gavage daily for 8 d.The rats in the control and HH groups were treated with the same volume of saline.The intestinal morphology,serum levels of malondialdehyde(MDA),superoxide dismutase(SOD),interleukin-6 (IL-6),tumor necrosis factor-α(TNF-α),interferon-gamma(IFN-γ)and diamino oxidase(DAO)were examined.We also evaluated the expression levels of occludin,toll-like receptor 4(TLR4),nuclear factor-κB p65(NF-κB p65)and myeloid differentiation factor 88(MyD88),and examined the bacterial community in caecal contents.RESULTS:Hypobaric hypoxia induced the enlargement of the heart,liver,lung and kidney,and caused spleen atrophy.Intestinal villi damage was also observed in the HH group.Supplementation with Gln significantly alleviated hypobaric-induced damage to main organs including the intestine,increased serum SOD(1.14±0.03 vs 0.88±0.04,P<0.05)and MDA(8.35±1.60,P<0.01)levels and decreased serum IL-6(1172.13±30.49 vs 1407.05±34.36,P<0.05),TNF-α(77.46±0.78 vs 123.70±3.03,P<0.001),IFN-γ(1355.42±72.80 vs 1830.16±42.07,P<0.01)and DAO(629.30±9.15 vs 524.10±13.34,P<0.001)levels.Moreover,Gln significantly increased occludin(0.72±0.05 vs 0.09±0.01,P<0.001),TLR4(0.15±0.05 vs 0.30±0.09,P<0.05),MyD88(0.32±0.08 vs 0.71±0.06,P<0.01),and NF-κB p65(0.16±0.04 vs 0.44±0.03,P<0.01)expression levels and improved the intestinal bacterial community.CONCLUSION:Gln treatment protects from intestinal injury and regulates the gut flora imbalance in hypoxia environment.These effects may be related to the TLR4/MyD88/NF-κB signaling pathway. | Chun-Lan Xu Rui Sun Xiang-Jin Qiao Cui-Cui Xu Xiao-Ya Shang Wei-Ning Niu | 2014 | World Journal of Gastroenterology2014，20，16： | 29 |
| 17 | Intestinal microbiota pathogenesis and fecal microbiota transplantation for inflammatory bowel disease显示文摘The intestinal microbiota plays an important role in inflammatory bowel disease(IBD).The pathogenesis of IBD involves inappropriate ongoing activation of the mucosal immune system driven by abnormal intestinal microbiota in genetically predisposed individuals.However,there are still no definitive microbial pathogens linked to the onset of IBD.The composition and function of the intestinal microbiota and their metabolites are indeed disturbed in IBD patients.The special alterations of gut microbiota associated with IBD remain to be evaluated.The microbial interactions and hostmicrobe immune interactions are still not clarified.Limitations of present probiotic products in IBD are mainly due to modest clinical efficacy,few available strains and no standardized administration.Fecal microbiota transplantation(FMT)may restore intestinal microbial ho-meostasis,and preliminary data have shown the clinical efficacy of FMT on refractory IBD or IBD combined with Clostridium difficile infection.Additionally,synthetic microbiota transplantation with the defined composition of fecal microbiota is also a promising therapeutic approach for IBD.However,FMT-related barriers,including the mechanism of restoring gut microbiota,standardized donor screening,fecal material preparation and administration,and long-term safety should be resolved.The role of intestinal microbiota and FMT in IBD should be further investigated by metagenomic and metatranscriptomic analyses combined with germfree/human flora-associated animals and chemostat gut models. | Zi-Kai Wang Yun-Sheng Yang Ye Chen Jing Yuan Gang Sun Li-Hua Peng | 2014 | World Journal of Gastroenterology2014，20，40： | 30 |
| 18 | Obesity, fatty liver disease and intestinal microbiota显示文摘Nonalcoholic fatty liver disease(NAFLD) is a chronic liver disorder that is increasing in prevalence with the worldwide epidemic of obesity. NAFLD is the hepatic manifestation of the metabolic syndrome. The term NAFLD describes a spectrum of liver pathology ranges from simple steatosis to steatosis with inflammation nonalcoholic steatohepatitis and even cirrhosis. Metabolic syndrome and NAFLD also predict hepatocellular carcinoma. Many genetic and environmental factors have been suggested to contribute to the development of obesity and NAFLD, but the exact mechanisms are not known. Intestinal ecosystem contains trillions of microorganisms including bacteria, Archaea, yeasts and viruses. Several studies support the relationship between the intestinal microbial changes and obesity and also its complications, including insulin resistance and NAFLD. Given that the gut and liver are connected by the portal venous system, it makes the liver more vulnerable to translocation of bacteria, bacterial products, endotoxins or secreted cytokines. Altered intestinal microbiota(dysbiosis) may stimulate hepatic fat deposition through several mechanisms: regulation of gut permeability, increasing low-grade inflammation, modulation of dietary choline metabolism, regulation of bile acid metabolism and producing endogenous ethanol. Regulation of intestinal microbial ecosystem by diet modifications or by using probiotics and prebiotics as a treatment for obesity and its complications might be the issue of further investigations. | Nur Arslan | 2014 | World Journal of Gastroenterology2014，20，44： | 30 |
| 19 | Accurate definition and management of idiopathic sclerosing encapsulating peritonitis显示文摘AIM: To review the literature on idiopathic sclerosing encapsulating peritonitis(SEP), also known as abdominal cocoon syndrome. METHODS: The Pub Med, MEDLINE, Google Scholar, and Google databases were searched using specific key words to identify articles related to idiopathic SEP. These key words were 'sclerosing encapsulating peritonitis,' 'idiopathic sclerosing encapsulating peritonitis,' 'abdominal cocoon,' and 'abdominal cocoon syndrome.' The search included letters tothe editor, case reports, review articles, original articles, and meeting presentations published in the English-language literature from January 2000 to May 2014. Articles or abstracts containing adequate information about age, sex, symptom duration, initial diagnosis, radiological tools, and surgical approaches were included in the study. Papers with missing or inadequate data were excluded. RESULTS: The literature search yielded 73 articles on idiopathic(primary) SEP published in 23 countries. The four countries that published the greatest number of articles were India(n = 21), Turkey(n = 14), China(n = 8) and Nigeria(n = 3). The four countries that reported the greatest number of cases were China(n = 104; 53.88%), India(n = 35; 18.13%), Turkey(n = 17; 8.80%) and Nigeria(n = 5; 2.59%). The present study included 193 patients. Data on age could be obtained for 184 patients(range: 7-87 years; mean ± SD, 34.7 ± 19.2 years), but were unavailable for nine patients. Of the 184 patients, 122 were male and 62 were female; sex data could not be accessed in the remaining nine patients. Of the 149 patients whose preoperative diagnosis information could be obtained, 65(43.6%) underwent operations for abdominal cocoon, while the majority of the remaining patients underwent operations for a presumed diagnosis of intestinal obstruction and/or abdominal mass. Management information could be retrieved for 115 patients. Of these, 68 underwent excision + adhesiolysis(one laparoscopic); 24 underwent prophylactic appendectomy in addition to excision + adhesiolysis. Twenty patients underwent various resection and repair techniques along with excision + adhesiolysis. The remaining three patients were managed with antituberculosis therapy(n = 2) and immunosuppressive therapy(n = 1). CONCLUSION: Idiopathic SEP is a rare disorder characterized by frequently recurring bouts of intestinal obstruction. Surgical therapy is the gold standardmanagement strategy. | Sami Akbulut | 2015 | World Journal of Gastroenterology2015，21，2： | 29 |
| 20 | Moxibustion regulates inflammatory mediators and colonic mucosal barrier in ulcerative colitis rats显示文摘AIM: To observe the efficacy and mechanism of grainsized moxibustion at different acupoints in a rat model of ulcerative colitis(UC). METHODS: Sprague-Dawley rats were randomly divided into control, UC model, grain-sized moxibustion at a single acupoint(CV 12), grain-sized moxibustion at two acupoints(CV 12 and CV 4), grain-sized moxibustion at three acupoints(CV 12, CV 4, and ST 36), and medication groups(n = 8/group). The UC model was established by enema of trinitrobenzene sulfonic acid. Direct moxibustion was used once a day for 7 d. Disease activity index(DAI) was evaluated before and after the treatment. Morphologic changes of intestinal tissue were observed under an optical microscope. The expression of tumor necrosis factor(TNF)-α and p38 mitogen-activated protein kinase(p38MAPK) in colonic tissue was detected using Western blot, and the levels of occludin and zonula occludens-1(ZO-1) m RNAs were detected using reverse transcription PCR. RESULTS: Compared with the control group, the intestinal mucosae were incomplete in the model group, glandular structures were irregular, and submucosae were edematous, hyperemic, and infiltrated with inflammatory cells. The DAI scores and expression ofTNF-α and p38 MAPK were increased significantly in the model group compared to controls(P s < 0.01), while the m RNA levels of occludin and ZO-1 were reduced significantly(P s < 0.01). Compared with the model group, colonic mucosa and the arrangement of glands were complete and regular in the treatment groups. DAI scores and the expression of TNF-α and p38 MAPK were reduced significantly in moxibustion groups compared to controls(P s < 0.01), while the m RNA levels of occludin and ZO-1 were increased significantly(P s < 0.01). The improvements in the above indices in the three acupoints group and the medication group were superior to those in the single and two acupoints groups(all P < 0.05). CONCLUSION: Reduction of TNF-α and p38 MAPK and increased expression of occludin and ZO-1 in colonic tissue represent a potential mechanism for improved intestinal mucosal tissue repair with grain-sized moxibustion. | Tie-Ming Ma Na Xu Xian-De Ma Zeng-Hua Bai Xing Tao Hong-Chi Yan | 2016 | World Journal of Gastroenterology2016，22，8： | 30 |
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