scholarly journals FAM3D is essential for colon homeostasis and host defense against inflammation associated carcinogenesis

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Weiwei Liang ◽  
Xinjian Peng ◽  
Qingqing Li ◽  
Pingzhang Wang ◽  
Ping Lv ◽  
...  
Keyword(s):  
Fecal Microbiota ◽  
Mucosal Barrier ◽  
Chemically Induced ◽  
Normal Microbiota ◽  
Physiological Homeostasis ◽  
Gut Mucosal Barrier ◽  
Increased Sensitivity ◽  
Inflammatory Bowel ◽  
Genetic And Environmental Factors

AbstractThe physiological homeostasis of gut mucosal barrier is maintained by both genetic and environmental factors and its impairment leads to pathogenesis such as inflammatory bowel disease. A cytokine like molecule, FAM3D (mouse Fam3D), is highly expressed in mouse gastrointestinal tract. Here, we demonstrate that deficiency in Fam3D is associated with impaired integrity of colonic mucosa, increased epithelial hyper-proliferation, reduced anti-microbial peptide production and increased sensitivity to chemically induced colitis associated with high incidence of cancer. Pretreatment of Fam3D−/− mice with antibiotics significantly reduces the severity of chemically induced colitis and wild type (WT) mice co-housed with Fam3D−/− mice phenocopy Fam3D-deficiency showing increased sensitivity to colitis and skewed composition of fecal microbiota. An initial equilibrium of microbiota in cohoused WT and Fam3D−/− mice is followed by an increasing divergence of the bacterial composition after separation. These results demonstrate the essential role of Fam3D in colon homeostasis, protection against inflammation associated cancer and normal microbiota composition.

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 Alterations of the Predominant Fecal Microbiota and Disruption of the Gut Mucosal Barrier in Patients with Early-Stage Colorectal Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Xia Liu ◽  
Yiwen Cheng ◽  
Li Shao ◽  
Zongxin Ling
Keyword(s):  
Colorectal Cancer ◽  
Diamine Oxidase ◽  
Early Stage ◽  
Fusobacterium Nucleatum ◽  
Fecal Microbiota ◽  
Mucosal Barrier ◽  
Beneficial Bacteria ◽  
Barrier Dysfunction ◽  
Real Time Quantitative Pcr ◽  
Gut Mucosal Barrier

Growing evidence indicated that the gut microbiota was the intrinsic and essential component of the cancer microenvironment, which played vital roles in the development and progression of colorectal cancer (CRC). In our present study, we investigated the alterations of fecal abundant microbiota with real-time quantitative PCR and the changes of indicators of gut mucosal barrier from 53 early-stage CRC patients and 45 matched healthy controls. We found that the traditional beneficial bacteria such as Lactobacillus and Bifidobacterium decreased significantly and the carcinogenic bacteria such as Enterobacteriaceae and Fusobacterium nucleatum were significantly increased in CRC patients. We also found gut mucosal barrier dysfunction in CRC patients with increased levels of endotoxin (LPS), D-lactate, and diamine oxidase (DAO). With Pearson’s correlation analysis, D-lactate, LPS, and DAO were correlated negatively with Lactobacillus and Bifidobacterium and positively with Enterobacteriaceae and F. nucleatum. Our present study found dysbiosis of the fecal microbiota and dysfunction of the gut mucosal barrier in patients with early-stage CRC, which implicated that fecal abundant bacteria and gut mucosal barrier indicators could be used as targets to monitor the development and progression of CRC in a noninvasive and dynamic manner.

scholarly journals Inflammatory Bowel Disease–Associated Changes in the Gut: Focus on Kazan Patients

2020 ◽  
Author(s):  
Giuseppe Lo Sasso ◽  
Lusine Khachatryan ◽  
Athanasios Kondylis ◽  
James N D Battey ◽  
Nicolas Sierro ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Redox Status ◽  
Fecal Microbiota ◽  
Whole Genome ◽  
Industrialized Countries ◽  
Newly Industrialized Countries ◽  
Inflammatory Bowel

Abstract Background Several studies have highlighted the role of host–microbiome interactions in the pathogenesis of inflammatory bowel disease (IBD), resulting in an increasing amount of data mainly focusing on Western patients. Because of the increasing prevalence of IBD in newly industrialized countries such as those in Asia, the Middle East, and South America, there is mounting interest in elucidating the gut microbiota of these populations. We present a comprehensive analysis of several IBD-related biomarkers and gut microbiota profiles and functions of a unique population of patients with IBD and healthy patients from Kazan (Republic of Tatarstan, Russia). Methods Blood and fecal IBD biomarkers, serum cytokines, and fecal short-chain fatty acid (SCFA) content were profiled. Finally, fecal microbiota composition was analyzed by 16S and whole-genome shotgun sequencing. Results Fecal microbiota whole-genome sequencing confirmed the presence of classic IBD dysbiotic features at the phylum level, with increased abundance of Proteobacteria, Actinobacteria, and Fusobacteria and decreased abundance of Firmicutes, Bacteroidetes, and Verrucomicrobia. At the genus level, the abundance of both fermentative (SCFA-producing and hydrogen (H2)-releasing) and hydrogenotrophic (H2-consuming) microbes was affected in patients with IBD. This imbalance was confirmed by the decreased abundance of SCFA species in the feces of patients with IBD and the change in anaerobic index, which mirrors the redox status of the intestine. Conclusions Our analyses highlighted how IBD-related dysbiotic microbiota—which are generally mainly linked to SCFA imbalance—may affect other important metabolic pathways, such as H2 metabolism, that are critical for host physiology and disease development.

scholarly journals Role of Th17 Cells in the Pathogenesis of Human IBD

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Julio Gálvez
Keyword(s):  
Th17 Cells ◽  
Current Knowledge ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Inflammatory Conditions ◽  
Normal Microbiota ◽  
Bowel Diseases ◽  
Mucosal Homeostasis ◽  
Inflammatory Bowel

The gastrointestinal tract plays a central role in immune system, being able to mount efficient immune responses against pathogens, keeping the homeostasis of the human gut. However, conditions like Crohn’s disease (CD) or ulcerative colitis (UC), the main forms of inflammatory bowel diseases (IBD), are related to an excessive and uncontrolled immune response against normal microbiota, through the activation of CD4+ T helper (Th) cells. Classically, IBD was thought to be primarily mediated by Th1 cells in CD or Th2 cells in UC, but it is now known that Th17 cells and their related cytokines are crucial mediators in both conditions. Th17 cells massively infiltrate the inflamed intestine of IBD patients, where they produce interleukin- (IL-) 17A and other cytokines, triggering and amplifying the inflammatory process. However, these cells show functional plasticity, and they can be converted into either IFN-γ producing Th1 cells or regulatory T cells. This review will summarize the current knowledge regarding the regulation and functional role of Th17 cells in the gut. Deeper insights into their plasticity in inflammatory conditions will contribute to advancing our understanding of the mechanisms that regulate mucosal homeostasis and inflammation in the gut, promoting the design of novel therapeutic approaches for IBD.

Fecal microbiota transplantation in gastrointestinal and extraintestinal disorders

2020 ◽  
Vol 15 (12) ◽  
pp. 1173-1183
Author(s):  
Gianluca Ianiro ◽  
Jonathan P Segal ◽  
Benjamin H Mullish ◽  
Mohammed N Quraishi ◽  
Serena Porcari ◽  
...  
Keyword(s):  
Fecal Microbiota Transplantation ◽  
Multidrug Resistant ◽  
Fecal Microbiota ◽  
Current Evidence ◽  
Resistant Bacteria ◽  
Clostridioides Difficile ◽  
Clostridioides Difficile Infection ◽  
Inflammatory Bowel ◽  
Irritable Bowel

Fecal microbiota transplantation (FMT) is the infusion of feces from a healthy donor into the gut of a recipient to treat a dysbiosis-related disease. FMT has been proven to be a safe and effective treatment for Clostridioides difficile infection, but increasing evidence supports the role of FMT in other gastrointestinal and extraintestinal diseases. The aim of this review is to paint the landscape of current evidence of FMT in different fields of application (including irritable bowel syndrome, inflammatory bowel disease, liver disorders, decolonization of multidrug-resistant bacteria, metabolic disorders and neurological disorders), as well as to discuss the current regulatory scenario of FMT, and hypothesize future directions of FMT.

Role of genetic and environmental factors in British twins with inflammatory bowel disease

2012 ◽  
Vol 18 (4) ◽  
pp. 725-736 ◽  
Author(s):  
Siew C. Ng ◽  
Susannah Woodrow ◽  
Nisha Patel ◽  
Javaid Subhani ◽  
Marcus Harbord
Keyword(s):  
Inflammatory Bowel Disease ◽  
Environmental Factors ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Genetic And Environmental Factors

scholarly journals Faecalibacterium prausnitzii: A Next-Generation Probiotic in Gut Disease Improvement

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Xiaoya He ◽  
Shuyang Zhao ◽  
Yan Li
Keyword(s):  
Fecal Microbiota Transplantation ◽  
Inflammatory Diseases ◽  
Symbiotic Bacterium ◽  
Fecal Microbiota ◽  
Next Generation ◽  
Faecalibacterium Prausnitzii ◽  
Inflammatory Bowel ◽  
Therapeutic Tools ◽  
Culture Strategy

The researchers are paying more attention to the role of gut commensal bacteria in health development beyond the classical pathogens. It has been widely demonstrated that dysbiosis, which means the alternations of the gut microbial structure, is closely associated with development of intestinal chronic inflammation-related diseases such as inflammatory bowel disease (IBD), and even infectious diseases including bacterial and viral infection. Thus, for reshaping ecological balance, a growing body of the literatures have proposed numerous strategies to modulate the structure of the gut microbiota, which provide more revelation for amelioration of these inflammation or infection-related diseases. While the ameliorative effects of traditional probiotics seem negligeable, emerging next generation probiotics (NGPs) start to receive great attention as new preventive and therapeutic tools. Encouragingly, within the last decade, the intestinal symbiotic bacterium Faecalibacterium prausnitzii has emerged as the “sentinel of the gut,” with multifunction of anti-inflammation, gut barrier enhancement, and butyrate production. A lower abundance of F. prausnitzii has been shown in IBD, Clostridium difficile infection (CDI), and virus infection such as COVID-19. It is reported that intervention with higher richness of F. prausnitzii through dietary modulation, fecal microbiota transplantation, or culture strategy can protect the mice or the subjects from inflammatory diseases. Therefore, F. prausnitzii may have potential ability to reduce microbial translocation and inflammation, preventing occurrences of gastrointestinal comorbidities especially in COVID-19 patients.

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.

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