scholarly journals Enterococcus faecium Alleviates Gut Barrier Injury in C57BL/6 Mice with Dextran Sulfate Sodium-Induced Ulcerative Colitis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Wei He ◽  
Weijie Ni ◽  
Junning Zhao
Keyword(s):  
Ulcerative Colitis ◽  
Enterococcus Faecium ◽  
Intestinal Flora ◽  
Underlying Mechanism ◽  
Mucosal Barrier ◽  
Microbiota Composition ◽  
Medicinal Value ◽  
Tnf Α ◽  
Inflammatory Bowel

The involvement of gut microbiota composition in ulcerative colitis is strongly supported by previous research. Growing evidence suggests that probiotic therapy protects against inflammatory bowel disease in animal models and patients. However, as a probiotic, the role of Enterococcus faecium (E. faecium) in UC remains unclear. Nevertheless, the potential mechanism of the protective effect of E. faecium remains unknown. In this study, a dextran sulphate sodium-induced (DSS-induced) colitis model was used to detect the underlying mechanism of E. faecium in maintaining gut homeostasis. ELISA was performed to detect the levels of cytokines (TNF-α, IL-1β, IL-6, and IL-10). Furthermore, 454 pyrosequencing was used to investigate the microbiota composition in fecal samples. The results illustrate that E. faecium administration could prevent DSS-induced gut inflammation and intestinal flora imbalance. At the same time, the damage to intestinal mucosal barrier and tight junctions was partially repaired. These results demonstrate the preventive effect of E. faecium in DSS-induced intestinal injury. The present study provides new insights into the medicinal value of E. faecium for UC.

scholarly journals The Role of Intestinal Dysbacteriosis Induced Arachidonic Acid Metabolism Disorder in Inflammaging in Atherosclerosis

2021 ◽  
Vol 11 ◽  
Author(s):  
Yingxin Sun ◽  
Danbin Wu ◽  
Wenyun Zeng ◽  
Yefei Chen ◽  
Maojuan Guo ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Intestinal Flora ◽  
Underlying Mechanism ◽  
Lesion Size ◽  
Arachidonic Acid Metabolism ◽  
The Other ◽  
Mucosal Barrier ◽  
Low Grade ◽  
Aged Mice

BackgroundAging induced chronic systemic inflammatory response is an important risk factor for atherosclerosis (AS) development; however, the detailed mechanism is yet to be elucidated.ObjectiveTo explore the underlying mechanism of how aging aggravates AS advancement.MethodsA young (five-week-old, YM) and aged group (32-week-old, OM) male apoE-/- mice with a high fat diet were used as models, and age-matched male wild-type C57BL/6J (WT) mice were used as controls. AS lesion size, serum lipid profile, cytokines, and gut microbiota-derived LPS were analyzed after 32 weeks of diet intervention. A correlation analysis between the 16S rRNA sequencing of the feces and serum metabolomics profiles was applied to examine the effect of their interactions on AS.ResultsApoE-/- mice developed severe atherosclerosis and inflammation in the aorta compared to the WT groups, and aged apoE-/- mice suffered from a more severe AS lesion than their younger counterparts and had low-grade systemic inflammation. Furthermore, increased levels of serum LPS, decreased levels of SCFAs production, as well as dysfunction of the ileal mucosal barrier were detected in aged mice compared with their younger counterparts. There were significant differences in the intestinal flora composition among the four groups, and harmful bacteria such as Lachnospiraceae_FCS020, Ruminococcaceae_UCG-009, Acetatifactor, Lachnoclostridium and Lactobacillus_gasseri were significantly increased in the aged apoE-/- mice compared with the other groups. Concurrently, metabolomics profiling revealed that components involved in the arachidonic acid (AA) metabolic pathway such as 20-HETE, PGF2α, arachidonic acid, and LTB4 were significantly higher in the aged AS group than in the other groups. This suggested that metabolic abnormalities and disorders of intestinal flora occurred in AS mice.ConclusionsAging not only altered the gut microbiome community but also substantially disturbed metabolic conditions. Our results confirm that AA metabolism is associated with the imbalance of the intestinal flora in the AS lesions of aged mice. These findings may offer new insights regarding the role of gut flora disorders and its consequent metabolite changed in inflammaging during AS development.

scholarly journals The role of TNF-alpha gene (-238G/A and -308G/A) polymorphisms in the etiology and pathogenesis of inflammatory bowel diseases in various ethnic groups

2019 ◽  
Vol 47 (6) ◽  
pp. 548-558
Author(s):  
I. V. Zhilin ◽  
E. Yu. Chashkova ◽  
A. A. Zhilina ◽  
B. S. Pushkarev ◽  
N. S. Korotaeva
Keyword(s):  
Ulcerative Colitis ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Gene Polymorphism ◽  
Ethnic Groups ◽  
Small Sample ◽  
Tnf Α ◽  
Study Results ◽  
Inflammatory Bowel

This literature review deals with specifics of the natural course of inflammatory bowel disease (IBD) in patients from various ethnic groups and -308G/A and -238G/A promoter polymorphisms in tumor necrosis factor-alpha (TNF-α) gene. The search in PubMed, Medline, Еlibrary.ru databases has led to identify in total 20 studies, including 2 meta-analyses, on the role of TNF-α-308G/A and -238G/A gene polymorphism in the etiology and pathophysiology of IBD. The TNF-α-308G/A polymorphism is associated with increased secretion of this proinflammatory cytokine, whereas the TNF-α-238G/A genotype is characterized by reduced TNF-α secretion. A  number of studies have shown an association between TNF-α-308G/A gene polymorphism and severe course of IBD, requiring more active treatment of patients (cytostatics, corticosteroids, biological agents). Some investigators have found that the patients carriers of TNF-α-308G/A had a  higher probability of surgical interventions. The association between TNF-α-308G/A and the phenotypic characteristics of IBD has been identified in studies performed in Europe, Asia, and Russia. The association of this polymorphism with the prevalence of ulcerative colitis has been proven in some studies, in particular, in the Asian population. Similar associations have been noted in few publications originating from Europe and North America, while some studies have found no links between TNF-α-308G/A, -238G/A, and the course of IBD. TNF-α-238G/A gene polymorphism has not shown any significance for the prevalence and course of ulcerative colitis and Crohn's disease. One can assume that the differences in the study results arising from one and the same geographical area are related to genetic heterogeneity of the study groups, phenotypic variances between the study subjects, as well as relatively small sample sizes. Currently, the search for genetic, biochemical and other prognostic criteria for IBD course is in progress. There are studies in progress to investigate the mechanisms of transformation of the genetic information into the particulars of ulcerative colitis and Crohn's disease manifestations, with consideration of ethnicity.

scholarly journals Microbiota-Immune Interactions in Ulcerative Colitis and Colitis Associated Cancer and Emerging Microbiota-Based Therapies

2021 ◽  
Vol 22 (21) ◽  
pp. 11365
Author(s):  
Jelena Popov ◽  
Valentina Caputi ◽  
Nandini Nandeesha ◽  
David Avelar Rodriguez ◽  
Nikhil Pai
Keyword(s):  
Ulcerative Colitis ◽  
Intestinal Inflammation ◽  
Autoimmune Disorder ◽  
Mucosal Barrier ◽  
Host Immune System ◽  
Intestinal Dysbiosis ◽  
Inflammatory Bowel ◽  
Genetic And Environmental Factors

Ulcerative colitis (UC) is a chronic autoimmune disorder affecting the colonic mucosa. UC is a subtype of inflammatory bowel disease along with Crohn’s disease and presents with varying extraintestinal manifestations. No single etiology for UC has been found, but a combination of genetic and environmental factors is suspected. Research has focused on the role of intestinal dysbiosis in the pathogenesis of UC, including the effects of dysbiosis on the integrity of the colonic mucosal barrier, priming and regulation of the host immune system, chronic inflammation, and progression to tumorigenesis. Characterization of key microbial taxa and their implications in the pathogenesis of UC and colitis-associated cancer (CAC) may present opportunities for modulating intestinal inflammation through microbial-targeted therapies. In this review, we discuss the microbiota-immune crosstalk in UC and CAC, as well as the evolution of microbiota-based therapies.

scholarly journals Role of Probiotics and Their Metabolites in Inflammatory Bowel Diseases (IBDs)

2021 ◽  
Vol 12 (1) ◽  
pp. 56-66
Author(s):  
Toumi Ryma ◽  
Arezki Samer ◽  
Imene Soufli ◽  
Hayet Rafa ◽  
Chafia Touil-Boukoffa
Keyword(s):  
Ulcerative Colitis ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Clinical Symptoms ◽  
Therapeutic Potential ◽  
Short Chain Fatty Acids ◽  
Active Metabolites ◽  
Complex Disorders ◽  
Inflammatory Bowel

Inflammatory Bowel Disease (IBD) is a term used to describe a group of complex disorders of the gastrointestinal (GI) tract. IBDs include two main forms: Crohn’s Disease (CD) and Ulcerative Colitis (UC), which share similar clinical symptoms but differ in the anatomical distribution of the inflammatory lesions. The etiology of IBDs is undetermined. Several hypotheses suggest that Crohn’s Disease and Ulcerative Colitis result from an abnormal immune response against endogenous flora and luminal antigens in genetically susceptible individuals. While there is no cure for IBDs, most common treatments (medication and surgery) aim to reduce inflammation and help patients to achieve remission. There is growing evidence and focus on the prophylactic and therapeutic potential of probiotics in IBDs. Probiotics are live microorganisms that regulate the mucosal immune system, the gut microbiota and the production of active metabolites such as Short-Chain Fatty Acids (SCFAs). This review will focus on the role of intestinal dysbiosis in the immunopathogenesis of IBDs and understanding the health-promoting effects of probiotics and their metabolites.

scholarly journals Inflammatory bowel disease: the role of inflammatory cytokine gene polymorphisms

2004 ◽  
Vol 13 (3) ◽  
pp. 181-187 ◽  
Author(s):  
Joanna Balding ◽  
Wendy J. Livingstone ◽  
Judith Conroy ◽  
Lesley Mynett-Johnson ◽  
Donald G. Weir ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Disease Incidence ◽  
Strong Association ◽  
Tnf Α ◽  
Genes Encoding ◽  
Inflammatory Processes ◽  
Inflammatory Bowel ◽  
Cytokine Gene Polymorphisms

THE mechanisms responsible for development of inflammatory bowel disease (IBD) have not been fully elucidated, although the main cause of disease pathology is attributed to up-regulated inflammatory processes. The aim of this study was to investigate frequencies of polymorphisms in genes encoding pro-inflammatory and anti-inflammatory markers in IBD patients and controls. We determined genotypes of patients with IBD (n=172) and healthy controls (n=389) for polymorphisms in genes encoding various cytokines (interleukin (IL)-1β, IL-6, tumour necrosis factor (TNF), IL-10, IL-1 receptor antagonist). Association of these genotypes to disease incidence and pathophysiology was investigated. No strong association was found with occurrence of IBD. Variation was observed between the ulcerative colitis study group and the control population for the TNF-α-308 polymorphism (p=0.0135). There was also variation in the frequency of IL-6-174 and TNF-α-308 genotypes in the ulcerative colitis group compared with the Crohn's disease group (p=0.01). We concluded that polymorphisms in inflammatory genes are associated with variations in IBD phenotype and disease susceptibility. Whether the polymorphisms are directly involved in regulating cytokine production, and consequently pathophysiology of IBD, or serve merely as markers in linkage disequilibrium with susceptibility genes remains unclear.

Hepatic dysfunction induced by intestinal dysbacteriosis mainly manifests as immunologic abnormity in mice

2020 ◽  
Vol 78 (6) ◽  
Author(s):  
Xia Luo ◽  
Bo Xu ◽  
Tianqin Xiong ◽  
Yulin Su ◽  
Chang liu ◽  
...  
Keyword(s):  
Potential Role ◽  
Hepatic Dysfunction ◽  
Intestinal Flora ◽  
Intestinal Wall ◽  
Mice Model ◽  
Intestinal Microbes ◽  
Transmission Electron ◽  
Tnf Α ◽  
Intestinal Dysbacteriosis

ABSTRACT Currently, the potential role of the alterations occurring in the liver immune system and intestinal flora in liver injury remains unknown. Our study aimed to explore the impacts of intestinal microbial barrier damage induced by ceftriaxone on liver immunity. We developed the BALB/c mice model by administering ceftriaxone. The intestinal microbial barrier damage was observed by 16S rRNA, and the pathological changes of intestines and livers were detected by H&E or transmission electron microscope. The activation of immunocytes were tested by Flow Cytometry; the expression of LPS, ALT, AST, IL-6 and TNF-α were detected by Limulus Test or ELISA. Compared to the control, the intestinal microbes significantly decreased in ceftriaxone group. Additionally, the weight of cecum contents increased, the intestinal wall became thinner and the villus in the small intestine and cecum were damaged. The expression of LPS and the ratio of liver lymphocytes were significantly increased. H&E results indicated the structures of liver arose the pathologic changes. Meanwhile, the content of serum ALT, AST, IL-6 and TNF-α increased. Collectively, our study indicates that the damages of gut microbial barrier induced by ceftriaxone prompted activation of immunocytes and release of inflammatory cytokines, which may lead to chronic inflammation in liver.

The Multifaceted Role of Natural Agents in Colitis-Associated Cancer Prevention and Therapy

2021 ◽  
pp. 220-239
Author(s):  
Ashok Kumar Kumar Pandurangan ◽  
Suresh Kumar Anandasadagopan ◽  
Neesar Ahmed
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Colon Cancer ◽  
The Other ◽  
Preclinical Model ◽  
Natural Agents ◽  
Inflammatory Bowel ◽  
Prevention And Therapy

Inflammatory bowel disease (IBD) is comprised of ulcerative colitis (UC) and Crohn's disease (CD) that was recognized by the inflammation in the colon. There are no proper medications are available to control the IBD in patients. NASIDs such as Aspirin, diclofenac, and ibuprofen are widely used to control the inflammation. On the other hand, the untreated prolonged inflammation leads to the development of cancer in the colon termed as colitis-associated cancer or inflammation-driven colon cancer. Oxidative stress and inflammation play key roles in the pathogenesis of colitis-associated cancer. Single dose of azozymethane (AOM) and three cycles of 2% dextran sodium sulfate (DSS) induces colitis-associated cancer (CAC) in mouse. Hence, many natural products were tested in the preclinical model of colitis-associated cancer. Each of these natural agents modulate important signaling pathway to control the colitis-associated cancer (CAC). In this review, the authors tabulated all the natural agents that culminate the colitis-associated cancer in the preclinical models.

Role of miR-19a targeting TNF-α in mediating ulcerative colitis

2013 ◽  
Vol 48 (7) ◽  
pp. 815-824 ◽  
Author(s):  
Bin Chen ◽  
Shifeng She ◽  
Detang Li ◽  
Zhihui Liu ◽  
Xiaojun Yang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Tnf Α

scholarly journals Tu1734 A Role of iRhom2 for the Secretion of TNF-α in Inflammatory Bowel Disease

2014 ◽  
Vol 146 (5) ◽  
pp. S-829 ◽  
Author(s):  
Sung Wook Hwang ◽  
Jaeyoung Chun ◽  
Changhyun Lee ◽  
Jong Pil Im ◽  
Joo Sung Kim
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Tnf Α ◽  
Inflammatory Bowel

scholarly journals Phosphatase Shp2 exacerbates intestinal inflammation by disrupting macrophage responsiveness to interleukin-10

2019 ◽  
Vol 216 (2) ◽  
pp. 337-349 ◽  
Author(s):  
Peng Xiao ◽  
Huilun Zhang ◽  
Yu Zhang ◽  
Mingzhu Zheng ◽  
Rongbei Liu ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Interleukin 10 ◽  
Blood Monocytes ◽  
Stat3 Signaling ◽  
Tnf Α ◽  
Mouse Macrophages ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
Further Development

Inflammatory cytokines produced by activated macrophages largely contribute to the pathological signs of inflammatory bowel disease (IBD). Interleukin-10 (IL-10) is the predominant anti-inflammatory cytokine in the intestine, and its therapeutic efficacy for IBD has been clinically tested. Nevertheless, how the function of IL-10 is regulated in the intestinal microenvironment remains unknown, which largely hinders the further development of IL-10–based therapeutic strategies. Here, we found that the expression of phosphatase Shp2 was increased in colonic macrophages and blood monocytes from IBD patients compared with those from healthy controls. Shp2 deficiency in macrophages protects mice from colitis and colitis-driven colon cancer. Mechanistically, Shp2 disrupts IL-10–STAT3 signaling and its dependent anti-inflammatory response in human and mouse macrophages. Furthermore, a Shp2-inducing role of TNF-α is unveiled in our study. Collectively, our work identifies Shp2 as a detrimental factor for intestinal immune homeostasis and hopefully will be helpful in the future exploitation of IL-10 immunotherapy for IBD.

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