World Journal of Gastrointestinal Pathophysiology最新文献

{"title":"Potential role of micro ribonucleic acids in screening for anal cancer in human papilloma virus and human immunodeficiency virus related malignancies.","authors":"Samar Al Bitar,&nbsp;Tala Ballouz,&nbsp;Samer Doughan,&nbsp;Hala Gali-Muhtasib,&nbsp;Nesrine Rizk","doi":"10.4291/wjgp.v12.i4.59","DOIUrl":"https://doi.org/10.4291/wjgp.v12.i4.59","url":null,"abstract":"<p><p>Despite advances in antiretroviral treatment (ART), human immunodeficiency virus (HIV) continues to be a major global public health issue owing to the increased mortality rates related to the prevalent oncogenic viruses among people living with HIV (PLWH). Human papillomavirus (HPV) is the most common sexually transmitted viral disease in both men and women worldwide. High-risk or oncogenic HPV types are associated with the development of HPV-related malignancies, including cervical, penile, and anal cancer, in addition to oral cancers. The incidence of anal squamous cell cancers is increasing among PLWH, necessitating the need for reliable screening methods in this population at risk. In fact, the currently used screening methods, including the Pap smear, are invasive and are neither sensitive nor specific. Investigators are interested in circulatory and tissue micro ribonucleic acids (miRNAs), as these small non-coding RNAs are ideal biomarkers for early detection and prognosis of cancer. Multiple miRNAs are deregulated during HIV and HPV infection and their deregulation contributes to the pathogenesis of disease. Here, we will review the molecular basis of HIV and HPV co-infections and focus on the pathogenesis and epidemiology of anal cancer in PLWH. The limitations of screening for anal cancer and the need for a reliable screening program that involves specific miRNAs with diagnostic and therapeutic values is also discussed.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"12 4","pages":"59-83"},"PeriodicalIF":0.0,"publicationDate":"2021-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5a/70/WJGP-12-59.PMC8316837.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39280523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet count as a screening tool for compensated cirrhosis in chronic viral hepatitis.","authors":"Pallavi Surana,&nbsp;Julian Hercun,&nbsp;Varun Takyar,&nbsp;David E Kleiner,&nbsp;Theo Heller,&nbsp;Christopher Koh","doi":"10.4291/wjgp.v12.i3.40","DOIUrl":"https://doi.org/10.4291/wjgp.v12.i3.40","url":null,"abstract":"<p><strong>Background: </strong>Simple tools for clinicians to identify cirrhosis in patients with chronic viral hepatitis are medically necessary for treatment initiation, hepatocellular cancer screening and additional medical management.</p><p><strong>Aim: </strong>To determine whether platelets or other laboratory markers can be used as a simple method to identify the development of cirrhosis.</p><p><strong>Methods: </strong>Clinical, biochemical and histologic laboratory data from treatment naive chronic viral hepatitis B (HBV), C (HCV), and D (HDV) patients at the NIH Clinical Center from 1985-2019 were collected and subjects were randomly divided into training and validation cohorts. Laboratory markers were tested for their ability to identify cirrhosis (Ishak ≥ 5) using receiver operating characteristic curves and an optimal cut-off was calculated within the training cohort. The final cut-off was tested within the validation cohort.</p><p><strong>Results: </strong>Overall, 1027 subjects (HCV = 701, HBV = 240 and HDV = 86), 66% male, with mean (standard deviation) age of 45 (11) years were evaluated. Within the training cohort (<i>n</i> = 715), platelets performed the best at identifying cirrhosis compared to other laboratory markers [Area Under the Receiver Operating Characteristics curve (AUROC) = 0.86 (0.82-0.90)] and sensitivity 77%, specificity 83%, positive predictive value 44%, and negative predictive value 95%. All other tested markers had AUROCs ≤ 0.77. The optimal platelet cut-off for detecting cirrhosis in the training cohort was 143 × 10⁹/L and it performed equally well in the validation cohort (<i>n</i> = 312) [AUROC = 0.85 (0.76-0.94)].</p><p><strong>Conclusion: </strong>The use of platelet counts should be considered to identify cirrhosis and ensure optimal care and management of patients with chronic viral hepatitis.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"12 3","pages":"40-50"},"PeriodicalIF":0.0,"publicationDate":"2021-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/38/29/WJGP-12-40.PMC8160599.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39058124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of cytomegalovirus reactivation just before liver transplantation: A prospective cohort study.","authors":"Claudio Marcel B Stadnik,&nbsp;Cassia Ferreira B Caurio,&nbsp;Edison M Rodrigues-Filho,&nbsp;Wagner L Nedel,&nbsp;Guido Pc Cantisani,&nbsp;Maria L Zanotelli,&nbsp;Alessandro C Pasqualotto","doi":"10.4291/wjgp.v12.i3.51","DOIUrl":"https://doi.org/10.4291/wjgp.v12.i3.51","url":null,"abstract":"<p><strong>Background: </strong>Cytomegalovirus (CMV) is the most common viral pathogen after liver transplantation (LT). Although reactivation of CMV infection is generally described in the context of immunosuppression, it has also been described in critically ill immunocompetent patients including cirrhotic patients.</p><p><strong>Aim: </strong>To determine the incidence of reactivated CMV prior to LT.</p><p><strong>Methods: </strong>This was a prospective cohort study evaluating adult patients who underwent LT between 2014 and 2016. A plasma sample was obtained from all patients for CMV quantitative real-time PCR testing right before transplantation. Patients were followed for at least 1 year to assess the following outcomes: Incidence of CMV infection, organ rejection and overall mortality.</p><p><strong>Results: </strong>A total of 72 patients were enrolled. Four patients died before transplantation, thus 68 patients were followed up for a median of 44 mo (20-50 mo). In 23/72 patients (31.9%) CMV was reactivated before transplantation. Post-transplantation, 16/68 (23.5%) patients had CMV infection and that was significantly associated with the recipient being CMV negative and a CMV-positive donor. Pre-transplant CMV reactivation was not associated with overall mortality (log rank: 0.9).</p><p><strong>Conclusion: </strong>This study shows that CMV infection is common in patients with chronic liver disease just before LT, but the clinical impact of this infection seems to be negligible.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"12 3","pages":"51-58"},"PeriodicalIF":0.0,"publicationDate":"2021-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/01/0b/WJGP-12-51.PMC8160598.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39058126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroimmunomodulation by gut bacteria: Focus on inflammatory bowel diseases.","authors":"Surbhi Aggarwal,&nbsp;Raju Ranjha,&nbsp;Jaishree Paul","doi":"10.4291/wjgp.v12.i3.25","DOIUrl":"https://doi.org/10.4291/wjgp.v12.i3.25","url":null,"abstract":"<p><p>Microbes colonize the gastrointestinal tract are considered as highest complex ecosystem because of having diverse bacterial species and 150 times more genes as compared to the human genome. Imbalance or dysbiosis in gut bacteria can cause dysregulation in gut homeostasis that subsequently activates the immune system, which leads to the development of inflammatory bowel disease (IBD). Neuromediators, including both neurotransmitters and neuropeptides, may contribute to the development of aberrant immune response. They are emerging as a regulator of inflammatory processes and play a key role in various autoimmune and inflammatory diseases. Neuromediators may influence immune cell's function <i>via</i> the receptors present on these cells. The cytokines secreted by the immune cells, in turn, regulate the neuronal functions by binding with their receptors present on sensory neurons. This bidirectional communication of the enteric nervous system and the enteric immune system is involved in regulating the magnitude of inflammatory pathways. Alterations in gut bacteria influence the level of neuromediators in the colon, which may affect the gastrointestinal inflammation in a disease condition. Changed neuromediators concentration <i>via</i> dysbiosis in gut microbiota is one of the novel approaches to understand the pathogenesis of IBD. In this article, we reviewed the existing knowledge on the role of neuromediators governing the pathogenesis of IBD, focusing on the reciprocal relationship among the gut microbiota, neuromediators, and host immunity. Understanding the neuromediators and host-microbiota interactions would give a better insight in to the disease pathophysiology and help in developing the new therapeutic approaches for the disease.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"12 3","pages":"25-39"},"PeriodicalIF":0.0,"publicationDate":"2021-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e8/36/WJGP-12-25.PMC8160600.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39058125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of non-alcoholic fatty liver disease with gallstone disease in the United States hospitalized patient population.","authors":"Asim Kichloo, Shantanu Solanki, Khwaja F Haq, Dushyant Dahiya, Beth Bailey, Dhanshree Solanki, Jagmeet Singh, Michael Albosta, Farah Wani, Michael Aljadah, Harshil Shah, Hafiz Khan, Syed-Mohammed Jafri","doi":"10.4291/wjgp.v12.i2.14","DOIUrl":"10.4291/wjgp.v12.i2.14","url":null,"abstract":"<p><strong>Background: </strong>Gallstones and cholecystectomy have been proposed as risk factors for non-alcoholic fatty liver disease (NAFLD). The reason for this may be that both gallstones, as well as NAFLD share several risk factors with regards to their development. Currently, there is a lack of sufficient evidence showing an association between these clinical conditions.</p><p><strong>Aim: </strong>To determine whether there is a meaningful association between gallstones and cholecystectomy with NAFLD.</p><p><strong>Methods: </strong>We queried the National Inpatient Sample database from the years 2016 and 2017 using International Classification of Diseases, 10^th revision, Clinical Modification diagnosis codes to identify hospitalizations with a diagnosis of gallstone disease (GSD) (includes calculus of gallbladder without cholecystitis without obstruction and acquired absence of gallbladder) as well as NAFLD (includes simple fatty liver and non-alcoholic steatohepatitis). Odds ratios (ORs) measuring the association between GSD (includes gallstones and cholecystectomy) and NAFLD were calculated using logistic regression after adjusting for confounding variables.</p><p><strong>Results: </strong>Out of 14294784 hospitalizations in 2016-2017, 159259 were found to have NAFLD. The prevalence of NAFLD was 3.3% in patients with GSD and 1% in those without. NAFLD was prevalent in 64.3% of women with GSD as compared to 35.7% of men with GSD. After controlling for various confounders associated with NAFLD and GSD, multivariate-adjusted analysis showed that there was an association between NAFLD with gallstones [OR = 6.32; 95% confidence interval (CI): 6.15-6.48] as well as cholecystectomy (OR = 1.97; 95%CI: 1.93-2.01). The association between NAFLD and gallstones was stronger in men (OR = 6.67; 95%CI: 6.42-6.93) than women (OR = 6.05; 95%CI: 5.83-6.27). The association between NAFLD and cholecystectomy was stronger in women (OR = 2.01; 95%CI: 1.96-2.06) than men (OR = 1.85; 95%CI: 1.79-1.92). <i>P</i> value was less than 0.001 for all comparisons.</p><p><strong>Conclusion: </strong>NAFLD is more prevalent in women with GSD than men. The association between NAFLD and cholecystectomy/gallstones indicates that they may be risk factors for NAFLD.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"12 2","pages":"14-24"},"PeriodicalIF":0.0,"publicationDate":"2021-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9b/a6/WJGP-12-14.PMC8008957.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25569454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of anastomoses on intestine ischemia and cefuroxime concentrations: Evaluated in the ileum and colon in a porcine model.","authors":"Pelle Hanberg,&nbsp;Mats Bue,&nbsp;Maja Thomassen,&nbsp;Uffe Schou Løve,&nbsp;Josephine Olsen Kipp,&nbsp;Christina Harlev,&nbsp;Elisabeth Petersen,&nbsp;Kjeld Søballe,&nbsp;Maiken Stilling","doi":"10.4291/wjgp.v12.i1.1","DOIUrl":"https://doi.org/10.4291/wjgp.v12.i1.1","url":null,"abstract":"<p><strong>Background: </strong>Anastomotic leakage is a serious complication following gastrointestinal surgery and is associated with increased morbidity and mortality. The incidence of anastomotic leakage is determined by anatomy and is reported to be between 4%-33% for colon anastomosis and 1%-3% for small intestine anastomosis. The etiology of anastomotic leakage of the intestine has been divided into three main factors: healing disturbances, communication between intra- and extra-luminal compartments, and infection. All three factors interact, and one factor will inevitably lead to the other two factors resulting in tissue ischemia, tissue necrosis, and anastomotic leakage.</p><p><strong>Aim: </strong>To evaluate ischemic metabolites and cefuroxime concentrations in both anastomosis and non-anastomosis ileum and colon in a porcine model.</p><p><strong>Methods: </strong>Eight healthy female pigs (Danish Landrace breed, weight 58-62 kg) were included in this study. Microdialysis catheters were placed for sampling of ischemic metabolites (glucose, lactate, glycerol, and pyruvate) and cefuroxime concentrations in both anastomosis and non-anastomosis ileum and colon. Cefuroxime 1.5 g was administered as an intravenous infusion over 15 min. Subsequently, dialysates and blood samples were collected over 8 h and the ischemic metabolites and cefuroxime concentrations were quantified in all samples. The concentrations of glucose, lactate, glycerol and pyruvate were determined using the CMA 600 Microdialysis Analyzer with Reagent Set A (M Dialysis AB, Sweden), and the concentrations of cefuroxime and meropenem were quantified using a validated ultra-high-performance liquid chromatography assay.</p><p><strong>Results: </strong>Only the colon anastomosis induced mean ischemic lactate/pyruvate ratios above 25 (ischemic cut-off) throughout the entire sampling interval, and simultaneously decreased glucose concentrations. The mean time for which cefuroxime concentrations were maintained above the clinical breakpoint minimal inhibitory concentration for <i>Escherichia coli</i> (8 µg/mL) ranged between 116-128 min across all the investigated compartments, and was similar between the anastomosis and non-anastomosis ileum and colon. For all pigs and in all the investigated compartments, a cefuroxime concentration of 8 µg/mL was reached within 10 min after administration. When comparing the pharmacokinetic parameters between the anastomosis and non-anastomosis sites for both ileum and colon, only colon T_max and half-life differed between anastomosis and non-anastomosis (<i>P</i> < 0.03). Incomplete tissue penetrations were found in all tissues except for the non-anastomosis colon.</p><p><strong>Conclusion: </strong>Administering 1.5 g cefuroxime 10 min prior to intestine surgery seems sufficient, and effective concentrations are sustained for approximately 2 h. Only colon anastomosis was locally vulnerable to ischemia.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"12 1","pages":"1-13"},"PeriodicalIF":0.0,"publicationDate":"2021-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ba/46/WJGP-12-1.PMC7852486.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25371875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical relevance of intestinal barrier dysfunction in common gastrointestinal diseases.","authors":"Andreas Muehler,&nbsp;Jason R Slizgi,&nbsp;Hella Kohlhof,&nbsp;Manfred Groeppel,&nbsp;Evelyn Peelen,&nbsp;Daniel Vitt","doi":"10.4291/wjgp.v11.i6.114","DOIUrl":"https://doi.org/10.4291/wjgp.v11.i6.114","url":null,"abstract":"<p><p>The intestinal barrier is a complex and well-controlled physiological construct designed to separate luminal contents from the bowel wall. In this review, we focus on the intestinal barrier's relationship with the host's immune system interaction and the external environment, specifically the microbiome. The bowel allows the host to obtain nutrients vital to survival while protecting itself from harmful pathogens, luminal antigens, or other pro-inflammatory factors. Control over barrier function and the luminal milieu is maintained at the biochemical, cellular, and immunological level. However, disruption to this highly regulated environment can cause disease. Recent advances to the field have progressed the mechanistic understanding of compromised intestinal barrier function in the context of gastrointestinal pathology. There are numerous examples where bowel barrier dysfunction and the resulting interaction between the microbiome and the immune system has disease-triggering consequences. The purpose of this review is to summarize the clinical relevance of intestinal barrier dysfunction in common gastrointestinal and related diseases. This may help highlight the importance of restoring barrier function as a therapeutic mechanism of action in gastrointestinal pathology.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"11 6","pages":"114-130"},"PeriodicalIF":0.0,"publicationDate":"2020-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/38/23/WJGP-11-114.PMC7739114.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38751746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atherosclerotic cardiovascular disease in inflammatory bowel disease: The role of chronic inflammation.","authors":"Simcha Weissman, Preetika Sinh, Tej I Mehta, Rishi K Thaker, Abraham Derman, Caleb Heiberger, Nabeel Qureshi, Viralkumar Amrutiya, Adam Atoot, Maneesh Dave, James H Tabibian","doi":"10.4291/wjgp.v11.i5.104","DOIUrl":"10.4291/wjgp.v11.i5.104","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) causes systemic vascular inflammation. The increased risk of venous as well as arterial thromboembolic phenomena in IBD is well established. More recently, a relationship between IBD and atherosclerotic cardiovascular disease (ASCVD) has been postulated. Systemic inflammatory diseases, such as rheumatoid arthritis and systemic lupus erythematosus, have well characterized cardiac pathologies and treatments that focus on prevention of disease associated ASCVD. The impact of chronic inflammation on ASCVD in IBD remains poorly characterized. This manuscript aims to review and summarize the current literature pertaining to IBD and ASCVD with respect to its pathophysiology and impact of medications in order to encourage further research that can improve understanding and help develop clinical recommendations for prevention and management of ASCVD in patients with IBD.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"11 5","pages":"104-113"},"PeriodicalIF":0.0,"publicationDate":"2020-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/58/78/WJGP-11-104.PMC7403753.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38293027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlations of morphology and molecular alterations in traditional serrated adenoma.","authors":"Hongxing Gui,&nbsp;Michael A Husson,&nbsp;Rifat Mannan","doi":"10.4291/wjgp.v11.i4.78","DOIUrl":"https://doi.org/10.4291/wjgp.v11.i4.78","url":null,"abstract":"<p><p>Traditional serrated adenoma was first reported by Longacre and Fenoglio-Presier in 1990. Their initial study described main features of this lesion, but the consensus diagnostic criteria were not widely adopted until recently. Traditional serrated adenoma presents with grossly protuberant configuration and pinecone-like appearance upon endoscopy. Histologically, it is characterized by ectopic crypt formation, slit-like serration, eosinophilic cytoplasm and pencillate nuclei. Although much is now known about the morphology and molecular changes, the mechanisms underlying the morphological alterations are still not fully understood. Furthermore, the origin of traditional serrated adenoma is not completely known. We review recent studies of the traditional serrated adenoma and provide an overview on current understanding of this rare entity.</p>","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"11 4","pages":"78-83"},"PeriodicalIF":0.0,"publicationDate":"2020-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a2/46/WJGP-11-78.PMC7303981.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38092487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X7 receptor antagonist recovers ileum myenteric neurons after experimental ulcerative colitis.","authors":"Roberta Figueiroa Souza,&nbsp;Mariá Munhoz Evangelinellis,&nbsp;Cristina Eusébio Mendes,&nbsp;Marta Righetti,&nbsp;Múcio Cevulla Silva Lourenço,&nbsp;Patricia Castelucci","doi":"10.4291/wjgp.v11.i4.84","DOIUrl":"https://doi.org/10.4291/wjgp.v11.i4.84","url":null,"abstract":"BACKGROUND The P2X7 receptor is expressed by enteric neurons and enteric glial cells. Studies have demonstrated that administration of a P2X7 receptor antagonist, brilliant blue G (BBG), prevents neuronal loss. AIM To report the effects of BBG in ileum enteric neurons immunoreactive (ir) following experimental ulcerative colitis in Rattus norvegicus albinus. METHODS 2,4,6-trinitrobenzene sulfonic acid (TNBS group, n = 5) was injected into the distal colon. BBG (50 mg/kg, BBG group, n = 5) or vehicle (sham group, n = 5) was given subcutaneously 1 h after TNBS. The animals were euthanized after 24 h, and the ileum was removed. Immunohistochemistry was performed on the myenteric plexus to evaluate immunoreactivity for P2X7 receptor, neuronal nitric oxide synthase (nNOS), choline acetyltransferase (ChAT), HuC/D and glial fibrillary acidic protein. RESULTS The numbers of nNOS-, ChAT-, HuC/D-ir neurons and glial fibrillary acidic protein-ir glial cells were decreased in the TNBS group and recovered in the BBG group. The neuronal profile area (μm2) demonstrated that nNOS-ir neurons decreased in the TNBS group and recovered in the BBG group. There were no differences in the profile areas of ChAT- and HuC/D-ir neurons. CONCLUSION Our data conclude that ileum myenteric neurons and glial cells were affected by ulcerative colitis and that treatment with BBG had a neuroprotective effect. Thus, these results demonstrate that the P2X7 receptor may be an important target in therapeutic strategies.","PeriodicalId":23760,"journal":{"name":"World Journal of Gastrointestinal Pathophysiology","volume":"11 4","pages":"84-103"},"PeriodicalIF":0.0,"publicationDate":"2020-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b7/6e/WJGP-11-84.PMC7303980.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38092488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}