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

Author(s):  
Giuseppe Lo Sasso ◽  
Lusine Khachatryan ◽  
Athanasios Kondylis ◽  
James N D Battey ◽  
Nicolas Sierro ◽  
...  

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.

2019 ◽  
Vol 156 (6) ◽  
pp. S-1124
Author(s):  
Clara Caenepeel ◽  
Sara Vieira-Silva ◽  
Jorge F. Vázquez-Castellanos ◽  
Bram Verstockt ◽  
Marc Ferrante ◽  
...  

2020 ◽  
Vol 11 (1) ◽  
pp. 119-143 ◽  
Author(s):  
Yanhui Han ◽  
Hang Xiao

Intake of whole foods, such as fruits and vegetables, may confer health benefits to the host. The beneficial effects of fruits and vegetables were mainly attributed to their richness in polyphenols and microbiota-accessible carbohydrates (MACs). Components in fruits and vegetables modulate composition and associated functions of the gut microbiota, whereas gut microbiota can transform components in fruits and vegetables to produce metabolites that are bioactive and important for health. The progression of multiple diseases, such as obesity and inflammatory bowel disease, is associated with diet and gut microbiota. Although the exact causality between these diseases and specific members of gut microbiota has not been well characterized, accumulating evidence supported the role of fruits and vegetables in modulating gut microbiota and decreasing the risks of microbiota-associated diseases. This review summarizes the latest findings on the effects of whole fruits and vegetables on gut microbiota and associated diseases.


2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S542-S542
Author(s):  
C Caenepeel ◽  
S Vieira-Silva ◽  
B Verstockt ◽  
M Ferrante ◽  
J Raes ◽  
...  

Pathogens ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 126 ◽  
Author(s):  
Israr Khan ◽  
Naeem Ullah ◽  
Lajia Zha ◽  
Yanrui Bai ◽  
Ashiq Khan ◽  
...  

Inflammatory bowel disease (IBD) is a chronic complex inflammatory gut pathological condition, examples of which include Crohn’s disease (CD) and ulcerative colitis (UC), which is associated with significant morbidity. Although the etiology of IBD is unknown, gut microbiota alteration (dysbiosis) is considered a novel factor involved in the pathogenesis of IBD. The gut microbiota acts as a metabolic organ and contributes to human health by performing various physiological functions; deviation in the gut flora composition is involved in various disease pathologies, including IBD. This review aims to summarize the current knowledge of gut microbiota alteration in IBD and how this contributes to intestinal inflammation, as well as explore the potential role of gut microbiota-based treatment approaches for the prevention and treatment of IBD. The current literature has clearly demonstrated a perturbation of the gut microbiota in IBD patients and mice colitis models, but a clear causal link of cause and effect has not yet been presented. In addition, gut microbiota-based therapeutic approaches have also shown good evidence of their effects in the amelioration of colitis in animal models (mice) and IBD patients, which indicates that gut flora might be a new promising therapeutic target for the treatment of IBD. However, insufficient data and confusing results from previous studies have led to a failure to define a core microbiome associated with IBD and the hidden mechanism of pathogenesis, which suggests that well-designed randomized control trials and mouse models are required for further research. In addition, a better understanding of this ecosystem will also determine the role of prebiotics and probiotics as therapeutic agents in the management of IBD.


2020 ◽  
Vol 117 (35) ◽  
pp. 21536-21545 ◽  
Author(s):  
Graham J. Britton ◽  
Eduardo J. Contijoch ◽  
Matthew P. Spindler ◽  
Varun Aggarwala ◽  
Belgin Dogan ◽  
...  

The building evidence for the contribution of microbiota to human disease has spurred an effort to develop therapies that target the gut microbiota. This is particularly evident in inflammatory bowel diseases (IBDs), where clinical trials of fecal microbiota transplantation have shown some efficacy. To aid the development of novel microbiota-targeted therapies and to better understand the biology underpinning such treatments, we have used gnotobiotic mice to model microbiota manipulations in the context of microbiotas from humans with inflammatory bowel disease. Mice colonized with IBD donor-derived microbiotas exhibit a stereotypical set of phenotypes, characterized by abundant mucosal Th17 cells, a deficit in the tolerogenic RORγt+regulatory T (Treg) cell subset, and susceptibility to disease in colitis models. Transplanting healthy donor-derived microbiotas into mice colonized with human IBD microbiotas led to induction of RORγt+Treg cells, which was associated with an increase in the density of the microbiotas following transplant. Microbiota transplant reduced gut Th17 cells in mice colonized with a microbiota from a donor with Crohn’s disease. By culturing strains from this microbiota and screening them in vivo, we identified a specific strain that potently induces Th17 cells. Microbiota transplants reduced the relative abundance of this strain in the gut microbiota, which was correlated with a reduction in Th17 cells and protection from colitis.


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