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Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 35897

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Dr. Silvia Melgar

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Guest Editor

APC Microbiome Ireland, University College Cork, T12 YT20 Cork, Ireland
Interests: inflammatory bowel disease (IBD); microbiota; inflammation; diets; epithelial cells; in vivo models; colon cancer
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Special Issue Information

Dear Colleagues,

In the last decade, the collected evidence indicates that the microbiota modulates the metabolic status, educates the host’s intestinal immune system, and protects the host against invading pathogens. Concomitantly, environmental factors such as diet have also been shown to shape the microbiota, thereby modulating the immune response and ultimately directing the health status of each individual. Therefore, disruptions in any of these three elements or their interactions have been linked to the development and progression of a number of intestinal inflammatory conditions including inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), celiac disease, colorectal cancer, etc. While Westernized diets rich in fat/sugar, low in fibers, and containing dietary additives such as emulsifiers have been linked to the development and progression of these disorders, other diets such as Mediterranean, ketogenic, and low-FODMAP, as well as dietary fiber supplementation, can potentially serve as treatment options due to their impact on the microbiota and on the host.

In this Special Issue, we welcome original research papers, reviews, short communications, and discussion papers addressing mechanisms regulated by diet, microbiota, and host interactions, revealing new cellular and immunological pathways targeted by bacteria and bacterial metabolites, diets, diet components, dietary additives, dietary fibers, etc. associated with intestinal health and disease.

Dr. Silvia Melgar
Guest Editor

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Keywords

diet
dietary additives and components
dietary fibers
westernized diet
intestinal inflammation
cancer
Immune system
epithelial cells
gut microbiota
bacterial metabolites

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Published Papers (8 papers)

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Research

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23 pages, 3986 KiB

Open AccessArticle

Dietary-Induced Bacterial Metabolites Reduce Inflammation and Inflammation-Associated Cancer via Vitamin D Pathway

by Caitlin O’Mahony, Adam Clooney, Siobhan F. Clarke, Mònica Aguilera, Aisling Gavin, Donjete Simnica, Mary Ahern, Aine Fanning, Maurice Stanley, Raul Cabrera Rubio, Elaine Patterson, Tatiana Marques, Rebecca Wall, Aileen Houston, Amr Mahmoud, Michael W. Bennett, Catherine Stanton, Marcus J. Claesson, Paul D. Cotter, Fergus Shanahan, Susan A. Joyce and Silvia Melgar Show full author list Hide full author list

Int. J. Mol. Sci. 2023, 24(3), 1864; https://doi.org/10.3390/ijms24031864 - 18 Jan 2023

Cited by 8 | Viewed by 3876

Abstract

Environmental factors, including westernised diets and alterations to the gut microbiota, are considered risk factors for inflammatory bowel diseases (IBD). The mechanisms underpinning diet-microbiota-host interactions are poorly understood in IBD. We present evidence that feeding a lard-based high-fat (HF) diet can protect mice from developing DSS-induced acute and chronic colitis and colitis-associated cancer (CAC) by significantly reducing tumour burden/incidence, immune cell infiltration, cytokine profile, and cell proliferation. We show that HF protection was associated with increased gut microbial diversity and a significant reduction in Proteobacteria and an increase in Firmicutes and Clostridium cluster XIVa abundance. Microbial functionality was modulated in terms of signalling fatty acids and bile acids (BA). Faecal secondary BAs were significantly induced to include moieties that can activate the vitamin D receptor (VDR), a nuclear receptor richly represented in the intestine and colon. Indeed, colonic VDR downstream target genes were upregulated in HF-fed mice and in combinatorial lipid-BAs-treated intestinal HT29 epithelial cells. Collectively, our data indicate that HF diet protects against colitis and CAC risk through gut microbiota and BA metabolites modulating vitamin D targeting pathways. Our data highlights the complex relationship between dietary fat-induced alterations of microbiota-host interactions in IBD/CAC pathophysiology. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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17 pages, 2371 KiB

Open AccessArticle

Fecal Luminal Factors from Patients with Gastrointestinal Diseases Alter Gene Expression Profiles in Caco-2 Cells and Colonoids

by Luiza Moraes Holst, Cristina Iribarren, Maria Sapnara, Otto Savolainen, Hans Törnblom, Yvonne Wettergren, Hans Strid, Magnus Simrén, Maria K. Magnusson and Lena Öhman

Int. J. Mol. Sci. 2022, 23(24), 15505; https://doi.org/10.3390/ijms232415505 - 7 Dec 2022

Cited by 6 | Viewed by 2630

Abstract

Previous in vitro studies have shown that the intestinal luminal content, including metabolites, possibly regulates epithelial layer responses to harmful stimuli and promotes disease. Therefore, we aimed to test the hypothesis that fecal supernatants from patients with colon cancer (CC), ulcerative colitis (UC) and irritable bowel syndrome (IBS) contain distinct metabolite profiles and establish their effects on Caco-2 cells and human-derived colon organoids (colonoids). The metabolite profiles of fecal supernatants were analyzed by liquid chromatography–mass spectrometry and distinguished patients with CC (n = 6), UC (n = 6), IBS (n = 6) and healthy subjects (n = 6). Caco-2 monolayers and human apical-out colonoids underwent stimulation with fecal supernatants from different patient groups and healthy subjects. Their addition did not impair monolayer integrity, as measured by transepithelial electrical resistance; however, fecal supernatants from different patient groups and healthy subjects altered the gene expression of Caco-2 monolayers, as well as colonoid cultures. In conclusion, the stimulation of Caco-2 cells and colonoids with fecal supernatants derived from CC, UC and IBS patients altered gene expression profiles, potentially reflecting the luminal microenvironment of the fecal sample donor. This experimental approach allows for investigating the crosstalk at the gut barrier and the effects of the gut microenvironment in the pathogenesis of intestinal diseases. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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20 pages, 3637 KiB

Open AccessArticle

Effect of Autolyzed Yarrowia lipolytica on the Growth Performance, Antioxidant Capacity, Intestinal Histology, Microbiota, and Transcriptome Profile of Juvenile Largemouth Bass (Micropterus salmoides)

by Hui Fei, Yan Cheng, Huimin Zhang, Xiang Yu, Shunfa Yi, Mengmeng Huang and Shun Yang

Int. J. Mol. Sci. 2022, 23(18), 10780; https://doi.org/10.3390/ijms231810780 - 15 Sep 2022

Cited by 11 | Viewed by 2309

Abstract

The improper components of formulated feed can cause the intestinal dysbiosis of juvenile largemouth bass and further affect fish health. A 28 day feeding trial was conducted to investigate the effect of partially replacing fish meal (FM) with autolyzed Yarrowia lipolytica (YL) on juvenile largemouth bass (Micropterus salmoides). We considered four diets—control, YL25, YL50, and YL75—in which 0%, 25%, 50%, and 75% of the FM content, respectively, was replaced with YL. According to results, the weight gain rate (WGR) and specific growth rate (SGR) of the fish with the YL25 and YL50 diets were significantly higher than the WGR and SGR with the control diet, while the YL75 diet significantly reduced fish growth and antioxidant enzymes activities, and shortened the villus height in the intestinal mucosa. The 16S rRNA analysis of the intestinal microbiota showed that the relative abundance of Mycoplasma was significantly increased with the YL25 and YL50 diets, while the Enterobacteriacea content was increased with the YL75 diet. Moreover, our transcriptome analysis revealed that certain differentially expressed genes (DEGs) that are associated with growth, metabolism, and immunity were modulated by YL inclusion treatment. Dietary YL25 and YL50 significantly reduced the mRNA level of ERBB receptor feedback inhibitor 1 (errfi1) and dual-specificity phosphatases (dusp), while the expression of the suppressor of cytokine signaling 1 (socs1), the transporter associated with antigen processing 2 subunit type a (tap2a), and the major histocompatibility complex class I-related gene (MHC-I-l) were sharply increased with YL75 treatment. We determined that the optimum dose of dietary YL required for maximum growth without any adverse influence on intestinal health was 189.82 g/kg (with 31.63% of the fishmeal replaced by YL), while an excessive substitution of YL for fishmeal led to suppressed growth and antioxidant capacity, as well as intestinal damage for juvenile largemouth bass. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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14 pages, 2558 KiB

Open AccessArticle

Betaine Alleviates High-Fat Diet-Induced Disruptionof Hepatic Lipid and Iron Homeostasis in Mice

by Yanlin Li, Wenduo Jiang, Yue Feng, Lei Wu, Yimin Jia and Ruqian Zhao

Int. J. Mol. Sci. 2022, 23(11), 6263; https://doi.org/10.3390/ijms23116263 - 3 Jun 2022

Cited by 20 | Viewed by 3518

Abstract

Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive fat deposition in the liver, which is often associated with disrupted iron homeostasis. Betaine has been reported to be hepatoprotective, yet whether and how betaine ameliorates high-fat diet-induced disruption of hepatic lipid and iron homeostasis remains elusive. In this study, mice were fed either standard (CON) or high-fat diet (HFD) for 9 weeks to establish a NAFLD model. Mice raised on HF diet were then assigned randomly to HF and HFB groups, HFB group being supplemented with 1% (w/v) of betaine in the drinking water for 13 weeks. Betaine supplementation significantly alleviated excessive hepatic lipid deposition and restored hepatic iron content. Betaine partly yet significantly reversed HFD-induced dysregulation of lipogenic genes such as PRAR

γ

and CD36, as well as the iron-metabolic genes including FPN and HAMP that encodes hepcidin. Similar mitigation effects of betaine were observed for BMP2 and BMP6, the up-stream regulators of hepcidin expression. Betaine significantly rectified disrupted expression of methyl transfer gene, including BHMT, GNMT and DNMT1. Moreover, HFD-modified CpG methylation on the promoter of PRAR

γ

and HAMP genes was significantly reversed by betaine supplementation. These results indicate that betaine alleviates HFD-induced disruption of hepatic lipid and iron metabolism, which is associated with modification of CpG methylation on promoter of lipogenic and iron-metabolic genes. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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19 pages, 5671 KiB

Open AccessArticle

Synbiotics Alleviate Hepatic Damage, Intestinal Injury and Muscular Beclin-1 Elevation in Rats after Chronic Ethanol Administration

by Yi-Hsiu Chen, Wan-Chun Chiu, Qian Xiao, Ya-Ling Chen, Hitoshi Shirakawa and Suh-Ching Yang

Int. J. Mol. Sci. 2021, 22(22), 12547; https://doi.org/10.3390/ijms222212547 - 21 Nov 2021

Cited by 7 | Viewed by 2140

Abstract

The purpose of this study was to investigate the beneficial effects of synbiotics on liver damage, intestinal health, and muscle loss, and their relevance in rats with chronic ethanol feeding. Thirty Wistar rats fed with a control liquid diet were divided into control and synbiotics groups, which were respectively provided with water or synbiotics solution (1.5 g/kg body weight/day) for 2 weeks. From the 3rd to 8th week, the control group was divided into a C group (control liquid diet + water) and an E group (ethanol liquid diet + water). The synbiotics group was separated in to three groups, SC, ASE, and PSE. The SC group was given a control liquid diet with synbiotics solution; the ASE group was given ethanol liquid diet with synbiotics solution, and the PSE group was given ethanol liquid diet and water. As the results, the E group exhibited liver damage, including increased AST and ALT activities, hepatic fatty changes, and higher CYP2E1 expression. Intestinal mRNA expressions of occludin and claudin-1 were significantly decreased and the plasma endotoxin level was significantly higher in the E group. In muscles, beclin-1 was significantly increased in the E group. Compared to the E group, the PSE and ASE groups had lower plasma ALT activities, hepatic fatty changes, and CYP2E1 expression. The PSE and ASE groups had significantly higher intestinal occludin and claudin-1 mRNA expressions and lower muscular beclin-1 expression when compared to the E group. In conclusion, synbiotics supplementation might reduce protein expression of muscle protein degradation biomarkers such as beclin-1 in rats with chronic ethanol feeding, which is speculated to be linked to the improvement of intestinal tight junction and the reduction of liver damage. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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Review

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19 pages, 5817 KiB

Open AccessReview

Crohn’s Disease, Host–Microbiota Interactions, and Immunonutrition: Dietary Strategies Targeting Gut Microbiome as Novel Therapeutic Approaches

by María A. Núñez-Sánchez, Silvia Melgar, Keith O’Donoghue, María A. Martínez-Sánchez, Virgina E. Fernández-Ruiz, Mercedes Ferrer-Gómez, Antonio J. Ruiz-Alcaraz and Bruno Ramos-Molina

Int. J. Mol. Sci. 2022, 23(15), 8361; https://doi.org/10.3390/ijms23158361 - 28 Jul 2022

Cited by 7 | Viewed by 4346

Abstract

Crohn’s disease (CD) is a complex, disabling, idiopathic, progressive, and destructive disorder with an unknown etiology. The pathogenesis of CD is multifactorial and involves the interplay between host genetics, and environmental factors, resulting in an aberrant immune response leading to intestinal inflammation. Due to the high morbidity and long-term management of CD, the development of non-pharmacological approaches to mitigate the severity of CD has recently attracted great attention. The gut microbiota has been recognized as an important player in the development of CD, and general alterations in the gut microbiome have been established in these patients. Thus, the gut microbiome has emerged as a pre-eminent target for potential new treatments in CD. Epidemiological and interventional studies have demonstrated that diet could impact the gut microbiome in terms of composition and functionality. However, how specific dietary strategies could modulate the gut microbiota composition and how this would impact host–microbe interactions in CD are still unclear. In this review, we discuss the most recent knowledge on host–microbe interactions and their involvement in CD pathogenesis and severity, and we highlight the most up-to-date information on gut microbiota modulation through nutritional strategies, focusing on the role of the microbiota in gut inflammation and immunity. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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17 pages, 2654 KiB

Open AccessReview

Diet–Microbiota Interplay: An Emerging Player in Macrophage Plasticity and Intestinal Health

by Cian O’Mahony, Asma Amamou and Subrata Ghosh

Int. J. Mol. Sci. 2022, 23(7), 3901; https://doi.org/10.3390/ijms23073901 - 31 Mar 2022

Cited by 13 | Viewed by 3892

Abstract

Inflammatory bowel diseases (IBD) are chronic disorders of the gastrointestinal tract with an increasing prevalence worldwide. Targeted therapies for IBD are limited by several factors, including the therapeutic ceiling and the high incidence of non-responders or loss-of-response. In order to improve therapeutic efficacy, there is critical need to decipher disease pathogenesis, currently not well understood. Macrophages, innate immune cells that exhibit high plasticity, perpetuate inflammatory signalling in IBD through excessive release of inflammatory mediators. In recent years, pioneering research has revealed the importance of the interplay between macrophages and gut microbiota in maintaining intestinal homeostasis. Particular attention is focusing on microbiota-derived metabolites, believed to possess immunomodulatory properties capable of manipulating macrophage plasticity. Microbiota-derived short-chain fatty acids (SCFAs) and indole compounds, along with dietary sourced omega-3 (ω-3) polyunsaturated fatty acids (PUFA), exert anti-inflammatory effects, attributable to interactions with macrophages. Before we can effectively incorporate these metabolites into IBD therapies, a deeper understanding of microbiota–macrophage interactions at a molecular level is necessary. Therefore, the aim of this review is firstly to detail current knowledge regarding how diet and microbiota-derived metabolites modify macrophage plasticity. Later, we discuss the concept of therapeutic strategies directed at microbiota–macrophage interactions, which could be highly valuable for IBD therapies in the future. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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23 pages, 1722 KiB

Open AccessReview

The Association between Gut Microbiota and Osteoarthritis: Does the Disease Begin in the Gut?

by Luciano C. Ramires, Gabriel Silva Santos, Rafaela Pereira Ramires, Lucas Furtado da Fonseca, Madhan Jeyaraman, Sathish Muthu, Anna Vitória Lana, Gabriel Azzini, Curtis Scott Smith and José Fábio Lana

Int. J. Mol. Sci. 2022, 23(3), 1494; https://doi.org/10.3390/ijms23031494 - 27 Jan 2022

Cited by 26 | Viewed by 12040

Abstract

Some say that all diseases begin in the gut. Interestingly, this concept is actually quite old, since it is attributed to the Ancient Greek physician Hippocrates, who proposed the hypothesis nearly 2500 years ago. The continuous breakthroughs in modern medicine have transformed our classic understanding of the gastrointestinal tract (GIT) and human health. Although the gut microbiota (GMB) has proven to be a core component of human health under standard metabolic conditions, there is now also a strong link connecting the composition and function of the GMB to the development of numerous diseases, especially the ones of musculoskeletal nature. The symbiotic microbes that reside in the gastrointestinal tract are very sensitive to biochemical stimuli and may respond in many different ways depending on the nature of these biological signals. Certain variables such as nutrition and physical modulation can either enhance or disrupt the equilibrium between the various species of gut microbes. In fact, fat-rich diets can cause dysbiosis, which decreases the number of protective bacteria and compromises the integrity of the epithelial barrier in the GIT. Overgrowth of pathogenic microbes then release higher quantities of toxic metabolites into the circulatory system, especially the pro-inflammatory cytokines detected in osteoarthritis (OA), thereby promoting inflammation and the initiation of many disease processes throughout the body. Although many studies link OA with GMB perturbations, further research is still needed. Full article

(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation 2.0)

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