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The Role of the Gut Microbiota in Inflammation and the Potential for Manipulation

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutritional Immunology".

Deadline for manuscript submissions: closed (15 October 2021) | Viewed by 15049

Special Issue Editor


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Guest Editor
Department of Microbiology, School of Genetics and Microbiology, Moyne Institute of Preventative Medicine, Trinity College Dublin, 2 Dublin, Ireland
Interests: microbiome; gut epithelial barrier; innate immunity; macrophage; inflammation; infection; IBD; therapeutics; diet; functional foods; pharmabiotics

Special Issue Information

Dear Colleagues,

Over the last decade, the field of microbiome research has exploded and our knowledge of the importance of the gut microbiome to intestinal health and wellbeing has increased significantly. The overall balance of the composition of the gut microbiota, as well as the contribution of key species and their metabolic by-products, is important in ensuring health, with microbiome disturbances being associated with the development of a range of diseases including nutrition-related disorders and chronic inflammation, inflammatory bowel disease (IBD), obesity, and metabolic syndrome.

This Special Issue will focus on the influence of the gut microbiota on intestinal health and the development of inflammation, and the possibility to therapeutically manipulate this relationship, with a specific focus on using functional food ingredients and dietary interventions to promote health. The aim of this Special Issue is to bring together recent research on these topics. Manuscripts that provide novel and mechanistic insights into the role of the microbiota in inflammation are encouraged.

Dr. Sinead Cristin Corr
Guest Editor

Manuscript Submission Information

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Keywords

  • Microbiome
  • Metabolites
  • Intestinal Epithelial Barrier
  • Inflammation
  • Therapeutic strategy
  • Functional Food ingredients
  • Diet
  • Postbiotics
  • Personalized Medicine

Published Papers (4 papers)

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Research

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18 pages, 3147 KiB  
Article
Preliminary Report on Intestinal Flora Disorder, Faecal Short-Chain Fatty Acid Level Decline and Intestinal Mucosal Tissue Weakening Caused by Litchi Extract to Induce Systemic Inflammation in HFA Mice
by Dongfang Sun, Chen Wang, Lijun Sun, Lianhua Hu, Zhijia Fang, Qi Deng, Jian Zhao and Ravi Gooneratne
Nutrients 2022, 14(4), 776; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14040776 - 12 Feb 2022
Cited by 2 | Viewed by 1740
Abstract
Certain foods are known as “heating” foods in Chinese medicine. Over-consumption of these foods can lead to symptoms known as “heating up”. These symptoms have been shown to be symptoms of systemic low-grade inflammation. However, the mechanism by which these foods cause inflammation [...] Read more.
Certain foods are known as “heating” foods in Chinese medicine. Over-consumption of these foods can lead to symptoms known as “heating up”. These symptoms have been shown to be symptoms of systemic low-grade inflammation. However, the mechanism by which these foods cause inflammation is not clear. In this preliminary study, we investigated dysbacteriosis of the gut microbiota as a possible cause of inflammation by litchi, a typical “heating” food. A human flora-associated (HFA) mouse model (donor: n = 1) was constructed. After gavaging the mice with litchi extract suspension at low, medium and high doses (400, 800, 1600 mg/kg·d−1, respectively) (n = 3) for 7 days, the serum levels of inflammatory cytokines, gut microbiota, the concentration of SCFAs and the integrity of the intestinal mucosal barrier were measured. The results revealed significant increases in the abundance of Prevotella and Bacteroides. A significant increase in the abundance of Bilophila and a decrease in Megasomonas was observed in the high-dose group. High-dose litchi intervention led to a decrease of most SCFA levels in the intestine. It also caused a more than two-fold increase in the serum TNF-α level and LPS level but a decrease in the IL-1β and IL-6 levels. Medium- and high-dose litchi intervention caused widening of the intestinal epithelial cell junction complex and general weakening of the intestinal mucosal barrier as well as reduced energy conversion efficiency of the gut microbiota. These data suggest that litchi, when consumed excessively, can lead to a low degree of systematic inflammation and this is linked to its ability to cause dysbacteriosis of the gut microbiota, decrease SCFAs and weaken the intestinal mucosal tissues. Full article
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14 pages, 4728 KiB  
Article
Dietary Barley Leaf Mitigates Tumorigenesis in Experimental Colitis-Associated Colorectal Cancer
by Daotong Li, Yu Feng, Meiling Tian, Xiaosong Hu, Ruimao Zheng and Fang Chen
Nutrients 2021, 13(10), 3487; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103487 - 30 Sep 2021
Cited by 6 | Viewed by 2671
Abstract
Dietary barley (Hordeum vulgare L.) leaf (BL) is a popular functional food known to have potential health benefits; however, the effect of BL in colorectal cancer prevention has not been examined. Here, we examined the role of BL on the prevention of [...] Read more.
Dietary barley (Hordeum vulgare L.) leaf (BL) is a popular functional food known to have potential health benefits; however, the effect of BL in colorectal cancer prevention has not been examined. Here, we examined the role of BL on the prevention of colorectal carcinogenesis and defined the mechanism involved. BL supplementation could protect against weight loss, mitigate tumor formation, and diminish histologic damage in mice treated with azoxymethane (AOM) and dextran sulfate sodium (DSS). Moreover, BL suppressed colonic expression of inflammatory enzymes, while improving the mucosal barrier dysfunctions. The elevated levels of cell proliferation markers and the increased expression of genes involved in β-catenin signaling were also reduced by BL. In addition, analyses of microbiota revealed that BL prevented AOM/DSS-induced gut microbiota dysbiosis by promoting the enrichment of Bifidobacterium. Overall, these data suggest that BL is a promising dietary agent for preventing colitis-associated colorectal cancer. Full article
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Review

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26 pages, 1023 KiB  
Review
Gut Microbial Metabolite-Mediated Regulation of the Intestinal Barrier in the Pathogenesis of Inflammatory Bowel Disease
by Namrata Iyer and Sinéad C. Corr
Nutrients 2021, 13(12), 4259; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124259 - 26 Nov 2021
Cited by 25 | Viewed by 5207
Abstract
Inflammatory bowel disease (IBD) is a chronic inflammatory disease. The disease has a multifactorial aetiology, involving genetic, microbial as well as environmental factors. The disease pathogenesis operates at the host–microbe interface in the gut. The intestinal epithelium plays a central role in IBD [...] Read more.
Inflammatory bowel disease (IBD) is a chronic inflammatory disease. The disease has a multifactorial aetiology, involving genetic, microbial as well as environmental factors. The disease pathogenesis operates at the host–microbe interface in the gut. The intestinal epithelium plays a central role in IBD disease pathogenesis. Apart from being a physical barrier, the epithelium acts as a node that integrates environmental, dietary, and microbial cues to calibrate host immune response and maintain homeostasis in the gut. IBD patients display microbial dysbiosis in the gut, combined with an increased barrier permeability that contributes to disease pathogenesis. Metabolites produced by microbes in the gut are dynamic indicators of diet, host, and microbial interplay in the gut. Microbial metabolites are actively absorbed or diffused across the intestinal lining to affect the host response in the intestine as well as at systemic sites via the engagement of cognate receptors. In this review, we summarize insights from metabolomics studies, uncovering the dynamic changes in gut metabolite profiles in IBD and their importance as potential diagnostic and prognostic biomarkers of disease. We focus on gut microbial metabolites as key regulators of the intestinal barrier and their role in the pathogenesis of IBD. Full article
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20 pages, 1272 KiB  
Review
Intestinal Microbiota as a Contributor to Chronic Inflammation and Its Potential Modifications
by Marta Potrykus, Sylwia Czaja-Stolc, Marta Stankiewicz, Łukasz Kaska and Sylwia Małgorzewicz
Nutrients 2021, 13(11), 3839; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13113839 - 28 Oct 2021
Cited by 28 | Viewed by 4661
Abstract
The gut microbiota is a crucial factor in maintaining homeostasis. The presence of commensal microorganisms leads to the stimulation of the immune system and its maturation. In turn, dysbiosis with an impaired intestinal barrier leads to accelerated contact of microbiota with the host’s [...] Read more.
The gut microbiota is a crucial factor in maintaining homeostasis. The presence of commensal microorganisms leads to the stimulation of the immune system and its maturation. In turn, dysbiosis with an impaired intestinal barrier leads to accelerated contact of microbiota with the host’s immune cells. Microbial structural parts, i.e., pathogen-associated molecular patterns (PAMPs), such as flagellin (FLG), peptidoglycan (PGN), lipoteichoic acid (LTA), and lipopolysaccharide (LPS), induce inflammation via activation of pattern recognition receptors. Microbial metabolites can also develop chronic low-grade inflammation, which is the cause of many metabolic diseases. This article aims to systematize information on the influence of microbiota on chronic inflammation and the benefits of microbiota modification through dietary changes, prebiotics, and probiotic intake. Scientific research indicates that the modification of the microbiota in various disease states can reduce inflammation and improve the metabolic profile. However, since there is no pattern for a healthy microbiota, there is no optimal way to modify it. The methods of influencing microbiota should be adapted to the type of dysbiosis. Although there are studies on the microbiota and its effects on inflammation, this subject is still relatively unknown, and more research is needed in this area. Full article
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