scholarly journals Modulating the microbiota in inflammatory bowel diseases: prebiotics, probiotics or faecal transplantation?

2014 ◽  
Vol 73 (4) ◽  
pp. 490-497 ◽  
Author(s):  
Kristin A. Verbeke ◽  
Leen Boesmans ◽  
Eef Boets

Crohn's disease (CD) and ulcerative colitis (UC) are the two major phenotypes of inflammatory bowel diseases (IBD) which constitute a spectrum of chronic, debilitating diseases characterised by a relapsing inflammation of the intestinal mucosal lining. Evidence from a variety of disciplines implicates the intestinal microbiota in the pathogenesis of idiopathic IBD and their complications, including pouchitis. Many studies have reported a dysbiosis in IBD, characterised by a decrease in diversity, a decreased abundance of some dominant commensal members (such asClostridiumIV and XIVa) and an increase in detrimental bacteria (such as sulphate reducing bacteria andEscherichia coli). Therapies such as prebiotics and probiotics aim to selectively manipulate the intestinal microbiota and have been evaluated as an attractive therapeutic option with few side effects. The multispecies product VSL#3 was found effective in preventing and maintaining remission in pouchitis, whereas both VSL#3 andE. coliNissle were effective in maintaining remission in UC. A more drastic approach to restore the composition of the microbiota and correct the underlying imbalance is a faecal microbiota transplantation (FMT). FMT has been successfully applied to treat patients with even recalcitrantClostridium difficileinfection. Particularly in UC, the majority of studies suggest that FMT may be an effective treatment option although the evidence is still limited. It is anticipated that our increasing knowledge on the composition and function of the intestinal microbiota components will allow in the future for a better selection of highly performing bacteria with specific functions required for specific benefits.

2021 ◽  
Vol 64 (9) ◽  
pp. 588-595
Author(s):  
Chang Soo Eun

Background: The prevalence of inflammatory bowel diseases (IBD) has been rapidly increasing over the past several decades in Korea. IBD appears to be resulted from inappropriate and chronic activation of the mucosal immune system driven by stimuli such as intestinal microbiota and various environmental factors in genetically susceptible individuals.Current Concepts: Recent advances in next-generation sequencing technology have identified alterations in the composition and function of the intestinal microbiota in individuals with IBD. Dysbiosis in patients with IBD is characterized by decreased bacterial diversity combined with an expansion of putative aggressive species and a reduction in protective species. Altered microbial composition and function in IBD correlates with increased immune stimulation, epithelial dysfunction, or enhanced mucosal permeability. Thus, dysbiosis may play an essential role in the pathogenesis of IBD.Discussion and Conclusion: Although it is currently unclear whether dysbiosis is a cause or consequence of intestinal inflammation in IBD, several microbial-based and microbial-targeted therapies have yielded promising early results.


2021 ◽  
Author(s):  
Lacey R. Lopez ◽  
Cassandra J. Barlogio ◽  
Christopher A. Broberg ◽  
Jeremy Wang ◽  
Janelle C. Arthur

AbstractInflammatory bowel diseases and inflammation-associated colorectal cancer are linked to blooms of adherent-invasive Escherichia coli (AIEC) in the intestinal microbiota. AIEC are functionally defined by their ability to adhere/invade epithelial cells and survive/replicate within macrophages. Changes in micronutrient availability can alter AIEC physiology and interactions with host cells. Thus, culturing AIEC for mechanistic investigations often involves precise nutrient formulation. We observed that the pro-inflammatory and pro-carcinogenic AIEC strain NC101 failed to grow in minimal media (MM). We hypothesized that NC101 was unable to synthesize a vital micronutrient normally found in the host gut. Through nutrient supplementation studies, we identified that NC101 is a nicotinic acid (NA) auxotroph. NA auxotrophy was not observed in the other non-toxigenic E. coli or AIEC strains we tested. Sequencing revealed NC101 has a missense mutation in nadA, a gene encoding quinolinate synthase A that is important for de novo NAD biosynthesis. Correcting the identified nadA point mutation restored NC101 prototrophy without impacting AIEC function, including motility and AIEC-defining survival in macrophages. Our findings, along with the generation of a prototrophic NC101 strain, will greatly enhance the ability to perform in vitro functional studies that are needed for mechanistic investigations on the role of intestinal E. coli in digestive disease.ImportanceInflammatory bowel diseases (IBD) and colorectal cancer (CRC) are significant global health concerns that are influenced by gut resident microbes, like adherent-invasive Escherichia coli (AIEC). Nutrient availability influences specialized metabolite production, AIEC-defining functional attributes, and AIEC:host interactions. NC101 is a pro-inflammatory and pro-carcinogenic AIEC strain commonly used for studies on IBD and CRC. We identified that NC101 growth in vitro requires a micronutrient found in the host gut. By correcting an identified mutation, we generated an NC101 strain that no longer has micronutrient restrictions. Our findings will facilitate future research that necessitates precise nutrient manipulation, enhancing AIEC functional studies and investigations on other auxotrophic intestinal microbiota members. Broadly, this will improve the study of bacterial:host interactions impacting health and disease.


2019 ◽  
Vol 10 (2) ◽  
pp. 1132-1145 ◽  
Author(s):  
Meiling Liu ◽  
Xiuxia Zhang ◽  
Yunpeng Hao ◽  
Jinhua Ding ◽  
Jing Shen ◽  
...  

Multiple articles have confirmed that an imbalance of the intestinal microbiota is closely related to aberrant immune responses of the intestines and to the pathogenesis of inflammatory bowel diseases (IBDs).


Immunology ◽  
2013 ◽  
Vol 139 (1) ◽  
pp. 100-108 ◽  
Author(s):  
Arwed Hostmann ◽  
Kerstin Kapp ◽  
Marianne Beutner ◽  
Jörg-Peter Ritz ◽  
Christoph Loddenkemper ◽  
...  

2019 ◽  
Vol 18 (1) ◽  
pp. 27-37
Author(s):  
Charilaos Triantafyllou ◽  
Maria Nikolaou ◽  
Ignatios Ikonomidis ◽  
Giorgos Bamias ◽  
Ioannis Papaconstantinou

Inflammatory bowel diseases (IBD), largely represented by Crohn’s disease (CD) and ulcerative colitis (UC), alter gastrointestinal physiology and mucosal immunity through a complex inflammatory process. These diseases can lead to significant arterial endothelial dysfunction. There is also evidence linking IBD with a modification of cardiac structure and function. A growing body of research has associated IBD with an acceleration of arterial stiffness and atherosclerosis and an increased risk of cardiovascular (CV) morbidity and mortality. The focus of this review is two-fold. Firstly, the literature on IBD in relation to CV dysfunction was evaluated (mainly based on 25 relevant surveys carried out between 2005 and 2018). The vast majority of these studies support a significant association of IBD with a deterioration in CV function. Secondly, the literature available regarding the effect of IBD treatment on CV dysfunction was considered based on studies published between 2007 and 2018. This literature search suggests that IBD treatment may have the potential to ameliorate CV dysfunction resulting in CV benefits. This review will analyse the literature as well as consider emerging research perspectives regarding how IBD treatment could improve CV dysfunction.


2020 ◽  
Vol 18 (9) ◽  
pp. 2019-2029.e11 ◽  
Author(s):  
Fabienne Humbel ◽  
Jessica Harrell Rieder ◽  
Yannick Franc ◽  
Pascal Juillerat ◽  
Michael Scharl ◽  
...  

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