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

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 (31 May 2021) | Viewed by 62249

Special Issue Editor

Dr. Silvia Melgar

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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 diets 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 and low in fibers, and dietary additives such as emulsifiers have been linked to the development and progression of these disorders, other diets such as Mediterranean, Ketogenic, Low-FODMAP, and dietary fibers 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, 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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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

Published Papers (18 papers)

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Research

Jump to: Review

16 pages, 2039 KiB  
Article
Inflammasome Signaling Regulates the Microbial–Neuroimmune Axis and Visceral Pain in Mice
by Mònica Aguilera, Valerio Rossini, Ana Hickey, Donjete Simnica, Fiona Grady, Valeria D. Felice, Amy Moloney, Lauren Pawley, Aine Fanning, Lorraine McCarthy, Siobhan M. O’Mahony, John F. Cryan, Ken Nally, Fergus Shanahan and Silvia Melgar
Int. J. Mol. Sci. 2021, 22(15), 8336; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158336 - 03 Aug 2021
Cited by 9 | Viewed by 3294
Abstract
Interactions between the intestinal microbiota, immune system and nervous system are essential for homeostasis in the gut. Inflammasomes contribute to innate immunity and brain–gut interactions, but their role in microbiota–neuro–immune interactions is not clear. Therefore, we investigated the effect of the inflammasome on [...] Read more.
Interactions between the intestinal microbiota, immune system and nervous system are essential for homeostasis in the gut. Inflammasomes contribute to innate immunity and brain–gut interactions, but their role in microbiota–neuro–immune interactions is not clear. Therefore, we investigated the effect of the inflammasome on visceral pain and local and systemic neuroimmune responses after antibiotic-induced changes to the microbiota. Wild-type (WT) and caspase-1/11 deficient (Casp1 KO) mice were orally treated for 2 weeks with an antibiotic cocktail (Abx, Bacitracin A and Neomycin), followed by quantification of representative fecal commensals (by qPCR), cecal short chain fatty acids (by HPLC), pathways implicated in the gut–neuro-immune axis (by RT-qPCR, immunofluorescence staining, and flow cytometry) in addition to capsaicin-induced visceral pain responses. Abx-treatment in WT-mice resulted in an increase in colonic macrophages, central neuro-immune interactions, colonic inflammasome and nociceptive receptor gene expression and a reduction in capsaicin-induced visceral pain. In contrast, these responses were attenuated in Abx-treated Casp1 KO mice. Collectively, the data indicate an important role for the inflammasome pathway in functional and inflammatory gastrointestinal conditions where pain and alterations in microbiota composition are prominent. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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20 pages, 8208 KiB  
Article
Sympathetic Denervation Alters the Inflammatory Response of Resident Muscularis Macrophages upon Surgical Trauma and Ameliorates Postoperative Ileus in Mice
by Shilpashree Mallesh, Reiner Schneider, Bianca Schneiker, Mariola Lysson, Patrik Efferz, Eugene Lin, Wouter J de Jonge and Sven Wehner
Int. J. Mol. Sci. 2021, 22(13), 6872; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22136872 - 26 Jun 2021
Cited by 11 | Viewed by 2472
Abstract
Interactions between the peripheral nervous system and resident macrophages (MMs) modulate intestinal homeostatic functions. Activation of β2-adrenergic receptors on MMs has been shown to reduce bacterial challenges. These MMs are also crucial for the development of bowel inflammation in postoperative ileus (POI), an [...] Read more.
Interactions between the peripheral nervous system and resident macrophages (MMs) modulate intestinal homeostatic functions. Activation of β2-adrenergic receptors on MMs has been shown to reduce bacterial challenges. These MMs are also crucial for the development of bowel inflammation in postoperative ileus (POI), an iatrogenic, noninfectious inflammation-based motility disorder. However, the role of the sympathetic nervous system (SNS) in the immune modulation of these MMs during POI or other noninfectious diseases is largely unknown. By employing 6-OHDA-induced denervation, we investigated the changes in the muscularis externa by RNA-seq, quantitative PCR, and flow cytometry. Further, we performed transcriptional phenotyping of sorted CX3CR1+ MMs and ex vivo LPS/M-CSF stimulation on these MMs. By combining denervation with a mouse POI model, we explored distinct changes on CX3CR1+ MMs as well as in the muscularis externa and their functional outcome during POI. Our results identify SNS as an important mediator in noninfectious postoperative inflammation. Upon denervation, MMs anti-inflammatory genes were reduced, and the muscularis externa profile is shaped toward a proinflammatory status. Further, denervation reduced MMs anti-inflammatory genes also in the early phase of POI. Finally, reduced leukocyte infiltration into the muscularis led to a quicker recovery of bowel motility in the late phase of POI. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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17 pages, 14902 KiB  
Article
Concentrated Raw Fibers Enhance the Fiber-Degrading Capacity of a Synthetic Human Gut Microbiome
by Alex Steimle, Mareike Neumann, Erica T. Grant, Jonathan D. Turner and Mahesh S. Desai
Int. J. Mol. Sci. 2021, 22(13), 6855; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22136855 - 25 Jun 2021
Cited by 4 | Viewed by 3681
Abstract
The consumption of prebiotic fibers to modulate the human gut microbiome is a promising strategy to positively impact health. Nevertheless, given the compositional complexity of the microbiome and its inter-individual variances, generalized recommendations on the source or amount of fiber supplements remain vague. [...] Read more.
The consumption of prebiotic fibers to modulate the human gut microbiome is a promising strategy to positively impact health. Nevertheless, given the compositional complexity of the microbiome and its inter-individual variances, generalized recommendations on the source or amount of fiber supplements remain vague. This problem is further compounded by availability of tractable in vitro and in vivo models to validate certain fibers. We employed a gnotobiotic mouse model containing a 14-member synthetic human gut microbiome (SM) in vivo, characterized a priori for their ability to metabolize a collection of fibers in vitro. This SM contains 14 different strains belonging to five distinct phyla. Since soluble purified fibers have been a common subject of studies, we specifically investigated the effects of dietary concentrated raw fibers (CRFs)—containing fibers from pea, oat, psyllium, wheat and apple—on the compositional and functional alterations in the SM. We demonstrate that, compared to a fiber-free diet, CRF supplementation increased the abundance of fiber-degraders, namely Eubacterium rectale, Roseburia intestinalis and Bacteroides ovatus and decreased the abundance of the mucin-degrader Akkermansia muciniphila. These results were corroborated by a general increase of bacterial fiber-degrading α-glucosidase enzyme activity. Overall, our results highlight the ability of CRFs to enhance the microbial fiber-degrading capacity. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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12 pages, 2247 KiB  
Article
(S)-Reutericyclin: Susceptibility Testing and In Vivo Effect on Murine Fecal Microbiome and Volatile Organic Compounds
by Bernhard Kienesberger, Beate Obermüller, Georg Singer, Barbara Mittl, Reingard Grabherr, Sigrid Mayrhofer, Stefan Heinl, Vanessa Stadlbauer, Angela Horvath, Wolfram Miekisch, Patricia Fuchs, Ingeborg Klymiuk, Holger Till and Christoph Castellani
Int. J. Mol. Sci. 2021, 22(12), 6424; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126424 - 15 Jun 2021
Cited by 3 | Viewed by 2259
Abstract
We aimed to assess the in vitro antimicrobial activity and the in vivo effect on the murine fecal microbiome and volatile organic compound (VOC) profile of (S)-reutericyclin. The antimicrobial activity of (S)-reutericyclin was tested against Clostridium difficile, Listeria monocytogenes, Escherichia coli [...] Read more.
We aimed to assess the in vitro antimicrobial activity and the in vivo effect on the murine fecal microbiome and volatile organic compound (VOC) profile of (S)-reutericyclin. The antimicrobial activity of (S)-reutericyclin was tested against Clostridium difficile, Listeria monocytogenes, Escherichia coli, Enterococcus faecium, Staphylococcus aureus, Staphylococcus (S.) epidermidis, Streptococcus agalactiae, Pseudomonas aeruginosa and Propionibacterium acnes. Reutericyclin or water were gavage fed to male BALBc mice for 7 weeks. Thereafter stool samples underwent 16S based microbiome analysis and VOC analysis by gas chromatography mass spectrometry (GC-MS). (S)-reutericyclin inhibited growth of S. epidermidis only. Oral (S)-reutericyclin treatment caused a trend towards reduced alpha diversity. Beta diversity was significantly influenced by reutericyclin. Linear discriminant analysis Effect Size (LEfSe) analysis showed an increase of Streptococcus and Muribaculum as well as a decrease of butyrate producing Ruminoclostridium, Roseburia and Eubacterium in the reutericyclin group. VOC analysis revealed significant increases of pentane and heptane and decreases of 2,3-butanedione and 2-heptanone in reutericyclin animals. The antimicrobial activity of (S)-reutericyclin differs from reports of (R)-reutericyclin with inhibitory effects on a multitude of Gram-positive bacteria reported in the literature. In vivo (S)-reutericyclin treatment led to a microbiome shift towards dysbiosis and distinct alterations of the fecal VOC profile. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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17 pages, 2550 KiB  
Article
Longitudinal Changes in Diet Cause Repeatable and Largely Reversible Shifts in Gut Microbial Communities of Laboratory Mice and Are Observed across Segments of the Entire Intestinal Tract
by Adrian Low, Melissa Soh, Sou Miyake, Vanessa Zhi Jie Aw, Jian Feng, Asher Wong and Henning Seedorf
Int. J. Mol. Sci. 2021, 22(11), 5981; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22115981 - 01 Jun 2021
Cited by 9 | Viewed by 2842
Abstract
Dietary changes are known to alter the composition of the gut microbiome. However, it is less understood how repeatable and reversible these changes are and how diet switches affect the microbiota in the various segments of the gastrointestinal tract. Here, a treatment group [...] Read more.
Dietary changes are known to alter the composition of the gut microbiome. However, it is less understood how repeatable and reversible these changes are and how diet switches affect the microbiota in the various segments of the gastrointestinal tract. Here, a treatment group of conventionally raised laboratory mice is subjected to two periods of western diet (WD) interrupted by a period of standard diet (SD) of the same duration. Beta-diversity analyses show that diet-induced microbiota changes are largely reversible (q = 0.1501; PERMANOVA, weighted-UniFrac comparison of the treatment-SD group to the control-SD group) and repeatable (q = 0.032; PERMANOVA, weighted-UniFrac comparison of both WD treatments). Furthermore, we report that diet switches alter the gut microbiota composition along the length of the intestinal tract in a segment-specific manner, leading to gut segment-specific Firmicutes/Bacteroidota ratios. We identified prevalent and distinct Amplicon Sequencing Variants (ASVs), particularly in genera of the recently described Muribaculaceae, along the gut as well as ASVs that are differentially abundant between segments of treatment and control groups. Overall, this study provides insights into the reversibility of diet-induced microbiota changes and highlights the importance of expanding sampling efforts beyond the collections of fecal samples to characterize diet-dependent and segment-specific microbiome differences. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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14 pages, 1969 KiB  
Article
Beneficial Effects of Natural Mineral Waters on Intestinal Inflammation and the Mucosa-Associated Microbiota
by Nicolas Barnich, Michael Rodrigues, Pierre Sauvanet, Caroline Chevarin, Sylvain Denis, Olivier Le Goff, Danielle Faure-Imbert, Thierry Hanh, Christian F Roques, Benoit Chassaing and Monique Alric
Int. J. Mol. Sci. 2021, 22(9), 4336; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094336 - 21 Apr 2021
Cited by 10 | Viewed by 3009
Abstract
Natural mineral water (NMWs) intake has been traditionally used in the treatment of various gastrointestinal diseases. We investigated the effect of two French NMWs, one a calcium and magnesium sulphate, sodium chloride, carbonic, and ferruginous water (NMW1), the other a mainly bicarbonate water [...] Read more.
Natural mineral water (NMWs) intake has been traditionally used in the treatment of various gastrointestinal diseases. We investigated the effect of two French NMWs, one a calcium and magnesium sulphate, sodium chloride, carbonic, and ferruginous water (NMW1), the other a mainly bicarbonate water (NMW2) on the prevention of intestinal inflammation. Intestinal epithelial cells stimulated with heat inactivated Escherichia coli or H2O2 were treated with NMWs to evaluate the anti-inflammatory effects. Moderate colitis was induced by 1% dextran sulfate sodium (DSS) in Balbc/J mice drinking NMW1, NWW2, or control water. General signs and histological features of colitis, fecal lipocalin-2 and pro-inflammatory KC cytokine levels, global mucosa-associated microbiota, were analyzed. We demonstrated that both NMW1 and NMW2 exhibited anti-inflammatory effects using intestinal cells. In induced-colitis mice, NMW1 was effective in dampening intestinal inflammation, with significant reductions in disease activity scores, fecal lipocalin-2 levels, pro-inflammatory KC cytokine release, and intestinal epithelial lesion sizes. Moreover, NMW1 was sufficient to prevent alterations in the mucosa-associated microbiota. These observations, through mechanisms involving modulation of the mucosa-associated microbiota, emphasize the need of investigation of the potential clinical efficiency of such NMWs to contribute, in human beings, to a state of low inflammation in inflammatory bowel disease. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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17 pages, 5702 KiB  
Article
Long-Term Iron Deficiency and Dietary Iron Excess Exacerbate Acute Dextran Sodium Sulphate-Induced Colitis and Are Associated with Significant Dysbiosis
by Awad Mahalhal, Michael D. Burkitt, Carrie A. Duckworth, Georgina L. Hold, Barry J. Campbell, David Mark Pritchard and Chris S. Probert
Int. J. Mol. Sci. 2021, 22(7), 3646; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073646 - 31 Mar 2021
Cited by 11 | Viewed by 2770
Abstract
Background: Oral iron supplementation causes gastrointestinal side effects. Short-term alterations in dietary iron exacerbate inflammation and alter the gut microbiota, in murine models of colitis. Patients typically take supplements for months. We investigated the impact of long-term changes in dietary iron on colitis [...] Read more.
Background: Oral iron supplementation causes gastrointestinal side effects. Short-term alterations in dietary iron exacerbate inflammation and alter the gut microbiota, in murine models of colitis. Patients typically take supplements for months. We investigated the impact of long-term changes in dietary iron on colitis and the microbiome in mice. Methods: We fed mice chow containing differing levels of iron, reflecting deficient (100 ppm), normal (200 ppm), and supplemented (400 ppm) intake for up to 9 weeks, both in absence and presence of dextran sodium sulphate (DSS)-induced chronic colitis. We also induced acute colitis in mice taking these diets for 8 weeks. Impact was assessed (i) clinically and histologically, and (ii) by sequencing the V4 region of 16S rRNA. Results: In mice with long-term changes, the iron-deficient diet was associated with greater weight loss and histological inflammation in the acute colitis model. Chronic colitis was not influenced by altering dietary iron however there was a change in the microbiome in DSS-treated mice consuming 100 ppm and 400 ppm iron diets, and control mice consuming the 400 ppm iron diet. Proteobacteria levels increased significantly, and Bacteroidetes levels decreased, in the 400 ppm iron DSS group at day-63 compared to baseline. Conclusions: Long-term dietary iron alterations affect gut microbiota signatures but do not exacerbate chronic colitis, however acute colitis is exacerbated by such dietary changes. More work is needed to understand the impact of iron supplementation on IBD. The change in the microbiome, in patients with colitis, may arise from the increased luminal iron and not simply from colitis. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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11 pages, 2595 KiB  
Article
Impaired Butyrate Induced Regulation of T Cell Surface Expression of CTLA-4 in Patients with Ulcerative Colitis
by Maria K. Magnusson, Alexander Vidal, Lujain Maasfeh, Stefan Isaksson, Rajneesh Malhotra, Henric K. Olsson and Lena Öhman
Int. J. Mol. Sci. 2021, 22(6), 3084; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063084 - 17 Mar 2021
Cited by 5 | Viewed by 2267
Abstract
Patients with ulcerative colitis (UC) have reduced intestinal levels of short-chain fatty acids (SCFAs), including butyrate, which are important regulators of host–microbiota crosstalk. The aim was therefore to determine effects of butyrate on blood and intestinal T cells from patients with active UC. [...] Read more.
Patients with ulcerative colitis (UC) have reduced intestinal levels of short-chain fatty acids (SCFAs), including butyrate, which are important regulators of host–microbiota crosstalk. The aim was therefore to determine effects of butyrate on blood and intestinal T cells from patients with active UC. T cells from UC patients and healthy subjects were polyclonally stimulated together with SCFAs and proliferation, activation, cytokine secretion, and surface expression of cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) were analyzed. Butyrate induced comparable, dose dependent inhibition of activation and proliferation in blood T cells and activation in intestinal T cells from UC patients and healthy subjects. However, surface expression of the inhibitory molecule CTLA-4 on stimulated blood and intestinal T cells was impaired in UC patients and was not restored following butyrate treatment. Furthermore, unlike intestinal T cells from healthy subjects, butyrate was unable to downregulate secretion of interferon gamma (IFNγ), interleukin (IL)-4, IL-17A, and IL-10 in UC patients. Although seemingly normal inhibitory effects on T cell activation and proliferation, butyrate has an impaired ability to reduce cytokine secretion and induce surface expression of CTLA-4 in T cells from UC patients with active disease. Overall, these observations indicate a dysfunction in butyrate induced immune regulation linked to CTLA-4 signaling in T cells from UC patients during a flare. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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15 pages, 7881 KiB  
Article
Momordica cochinchinensis Aril Ameliorates Diet-Induced Metabolic Dysfunction and Non-Alcoholic Fatty Liver by Modulating Gut Microbiota
by Hsiu-Chen Huang, Chiung-Ju Chen, Yu-Heng Lai, Yu-Chun Lin, Wei-Chung Chiou, Hsu-Feng Lu, Ying-Fang Chen, Yu-Hsin Chen and Cheng Huang
Int. J. Mol. Sci. 2021, 22(5), 2640; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052640 - 05 Mar 2021
Cited by 3 | Viewed by 2886
Abstract
Obesity and its associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are a particular worldwide health problem at present. Momordica cochinchinensis (MC) is consumed widely in Southeast Asia. However, whether it has functional effects on fat-induced [...] Read more.
Obesity and its associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are a particular worldwide health problem at present. Momordica cochinchinensis (MC) is consumed widely in Southeast Asia. However, whether it has functional effects on fat-induced metabolic syndrome remains unclear. This study was conducted to examine the prevention effect of Momordica cochinchinensis aril (MCA) on obesity, non-alcoholic fatty liver and insulin resistance in mice. MCA protected the mice against high-fat diet (HFD)-induced body weight gain, hyperlipidemia and hyperglycemia, compared with mice that were not treated. MCA inhibited the expansion of adipose tissue and adipocyte hypertrophy. In addition, the insulin sensitivity-associated index that evaluates insulin function was also significantly restored. MCA also regulated the secretion of adipokines in HFD-induced obese mice. Moreover, hepatic fat accumulation and liver damage were reduced, which suggested that fatty liver was prevented by MCA. Furthermore, MCA supplementation suppressed hepatic lipid accumulation by activation of the AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) signaling pathway in the human fatty liver HuS-E/2 cell model. Our data indicate that MCA altered the microbial contents of the gut and modulated microbial dysbiosis in the host, and consequently is involved in the prevention of HFD-induced adiposity, insulin resistance and non-alcoholic fatty liver disease. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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19 pages, 2136 KiB  
Article
Effects of Rifaximin on Luminal and Wall-Adhered Gut Commensal Microbiota in Mice
by Marina Ferrer, Mònica Aguilera and Vicente Martinez
Int. J. Mol. Sci. 2021, 22(2), 500; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020500 - 06 Jan 2021
Cited by 2 | Viewed by 2309
Abstract
Rifaximin is a broad-spectrum antibiotic that ameliorates symptomatology in inflammatory/functional gastrointestinal disorders. We assessed changes in gut commensal microbiota (GCM) and Toll-like receptors (TLRs) associated to rifaximin treatment in mice. Adult C57BL/6NCrl mice were treated (7/14 days) with rifaximin (50/150 mg/mouse/day, PO). Luminal [...] Read more.
Rifaximin is a broad-spectrum antibiotic that ameliorates symptomatology in inflammatory/functional gastrointestinal disorders. We assessed changes in gut commensal microbiota (GCM) and Toll-like receptors (TLRs) associated to rifaximin treatment in mice. Adult C57BL/6NCrl mice were treated (7/14 days) with rifaximin (50/150 mg/mouse/day, PO). Luminal and wall-adhered ceco-colonic GCM were characterized by fluorescent in situ hybridization (FISH) and microbial profiles determined by terminal restriction fragment length polymorphism (T-RFLP). Colonic expression of TLR2/3/4/5/7 and immune-related markers was assessed (RT-qPCR). Regardless the period of treatment or the dose, rifaximin did not alter total bacterial counts or bacterial biodiversity. Only a modest increase in Bacteroides spp. (150 mg/1-week treatment) was detected. In control conditions, only Clostridium spp. and Bifidobacterium spp. were found attached to the colonic epithelium. Rifaximin showed a tendency to favour their adherence after a 1-week, but not 2-week, treatment period. Minor up-regulation in TLRs expression was observed. Only the 50 mg dose for 1-week led to a significant increase (by 3-fold) in TLR-4 expression. No changes in the expression of immune-related markers were observed. Rifaximin, although its antibacterial properties, induces minor changes in luminal and wall-adhered GCM in healthy mice. Moreover, no modulation of TLRs or local immune systems was observed. These findings, in normal conditions, do not rule out a modulatory role of rifaximin in inflammatory and or dysbiotic states of the gut. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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16 pages, 3242 KiB  
Article
Histamine H2-Receptor Antagonists Improve Non-Steroidal Anti-Inflammatory Drug-Induced Intestinal Dysbiosis
by Rei Kawashima, Shun Tamaki, Fumitaka Kawakami, Tatsunori Maekawa and Takafumi Ichikawa
Int. J. Mol. Sci. 2020, 21(21), 8166; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218166 - 31 Oct 2020
Cited by 12 | Viewed by 2745
Abstract
Dysbiosis, an imbalance of intestinal flora, can cause serious conditions such as obesity, cancer, and psychoneurological disorders. One cause of dysbiosis is inflammation. Ulcerative enteritis is a side effect of non-steroidal anti-inflammatory drugs (NSAIDs). To counteract this side effect, we proposed the concurrent [...] Read more.
Dysbiosis, an imbalance of intestinal flora, can cause serious conditions such as obesity, cancer, and psychoneurological disorders. One cause of dysbiosis is inflammation. Ulcerative enteritis is a side effect of non-steroidal anti-inflammatory drugs (NSAIDs). To counteract this side effect, we proposed the concurrent use of histamine H2 receptor antagonists (H2RA), and we examined the effect on the intestinal flora. We generated a murine model of NSAID-induced intestinal mucosal injury, and we administered oral H2RA to the mice. We collected stool samples, compared the composition of intestinal flora using terminal restriction fragment length polymorphism, and performed organic acid analysis using high-performance liquid chromatography. The intestinal flora analysis revealed that NSAID [indomethacin (IDM)] administration increased Erysipelotrichaceae and decreased Clostridiales but that both had improved with the concurrent administration of H2RA. Fecal levels of acetic, propionic, and n-butyric acids increased with IDM administration and decreased with the concurrent administration of H2RA. Although in NSAID-induced gastroenteritis the proportion of intestinal microorganisms changes, leading to the deterioration of the intestinal environment, concurrent administration of H2RA can normalize the intestinal flora. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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Review

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25 pages, 1422 KiB  
Review
The Impact of Gut Microbiota-Derived Metabolites in Autism Spectrum Disorders
by Lucía N. Peralta-Marzal, Naika Prince, Djordje Bajic, Léa Roussin, Laurent Naudon, Sylvie Rabot, Johan Garssen, Aletta D. Kraneveld and Paula Perez-Pardo
Int. J. Mol. Sci. 2021, 22(18), 10052; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221810052 - 17 Sep 2021
Cited by 23 | Viewed by 5824
Abstract
Autism Spectrum Disorder (ASD) is a set of neurodevelopmental disorders characterised by behavioural impairment and deficiencies in social interaction and communication. A recent study estimated that 1 in 89 children have developed some form of ASD in European countries. Moreover, there is no [...] Read more.
Autism Spectrum Disorder (ASD) is a set of neurodevelopmental disorders characterised by behavioural impairment and deficiencies in social interaction and communication. A recent study estimated that 1 in 89 children have developed some form of ASD in European countries. Moreover, there is no specific treatment and since ASD is not a single clinical entity, the identification of molecular biomarkers for diagnosis remains challenging. Besides behavioural deficiencies, individuals with ASD often develop comorbid medical conditions including intestinal problems, which may reflect aberrations in the bidirectional communication between the brain and the gut. The impact of faecal microbial composition in brain development and behavioural functions has been repeatedly linked to ASD, as well as changes in the metabolic profile of individuals affected by ASD. Since metabolism is one of the major drivers of microbiome–host interactions, this review aims to report emerging literature showing shifts in gut microbiota metabolic function in ASD. Additionally, we discuss how these changes may be involved in and/or perpetuate ASD pathology. These valuable insights can help us to better comprehend ASD pathogenesis and may provide relevant biomarkers for improving diagnosis and identifying new therapeutic targets. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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24 pages, 8470 KiB  
Review
Microbiota Signals during the Neonatal Period Forge Life-Long Immune Responses
by Bryan Phillips-Farfán, Fernando Gómez-Chávez, Edgar Alejandro Medina-Torres, José Antonio Vargas-Villavicencio, Karla Carvajal-Aguilera and Luz Camacho
Int. J. Mol. Sci. 2021, 22(15), 8162; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158162 - 29 Jul 2021
Cited by 8 | Viewed by 3012
Abstract
The microbiota regulates immunological development during early human life, with long-term effects on health and disease. Microbial products include short-chain fatty acids (SCFAs), formyl peptides (FPs), polysaccharide A (PSA), polyamines (PAs), sphingolipids (SLPs) and aryl hydrocarbon receptor (AhR) ligands. Anti-inflammatory SCFAs are produced [...] Read more.
The microbiota regulates immunological development during early human life, with long-term effects on health and disease. Microbial products include short-chain fatty acids (SCFAs), formyl peptides (FPs), polysaccharide A (PSA), polyamines (PAs), sphingolipids (SLPs) and aryl hydrocarbon receptor (AhR) ligands. Anti-inflammatory SCFAs are produced by Actinobacteria, Bacteroidetes, Firmicutes, Spirochaetes and Verrucomicrobia by undigested-carbohydrate fermentation. Thus, fiber amount and type determine their occurrence. FPs bind receptors from the pattern recognition family, those from commensal bacteria induce a different response than those from pathogens. PSA is a capsular polysaccharide from B. fragilis stimulating immunoregulatory protein expression, promoting IL-2, STAT1 and STAT4 gene expression, affecting cytokine production and response modulation. PAs interact with neonatal immunity, contribute to gut maturation, modulate the gut–brain axis and regulate host immunity. SLPs are composed of a sphingoid attached to a fatty acid. Prokaryotic SLPs are mostly found in anaerobes. SLPs are involved in proliferation, apoptosis and immune regulation as signaling molecules. The AhR is a transcription factor regulating development, reproduction and metabolism. AhR binds many ligands due to its promiscuous binding site. It participates in immune tolerance, involving lymphocytes and antigen-presenting cells during early development in exposed humans. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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15 pages, 588 KiB  
Review
Dietary Habits and Gut Microbiota in Healthy Adults: Focusing on the Right Diet. A Systematic Review
by Giulia Gibiino, Martina De Siena, Monica Sbrancia, Cecilia Binda, Vittorio Sambri, Antonio Gasbarrini and Carlo Fabbri
Int. J. Mol. Sci. 2021, 22(13), 6728; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22136728 - 23 Jun 2021
Cited by 19 | Viewed by 3573
Abstract
Diet is the first to affect our intestinal microbiota and therefore the state of eubiosis. Several studies are highlighting the potential benefits of taking certain nutritional supplements, but a dietary regime that can ensure the health of the intestinal microbiota, and the many [...] Read more.
Diet is the first to affect our intestinal microbiota and therefore the state of eubiosis. Several studies are highlighting the potential benefits of taking certain nutritional supplements, but a dietary regime that can ensure the health of the intestinal microbiota, and the many pathways it governs, is not yet clearly defined. We performed a systematic review of the main studies concerning the impact of an omnivorous diet on the composition of the microbiota and the production of short-chain fatty acids (SCFAs). Some genera and phyla of interest emerged significantly and about half of the studies evaluated consider them to have an equally significant impact on the production of SCFAs, to be a source of nutrition for our colon cells, and many other processes. Although numerous randomized trials are still needed, the Mediterranean diet could play a valuable role in ensuring our health through direct interaction with our microbiota. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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18 pages, 326 KiB  
Review
Diet-Regulating Microbiota and Host Immune System in Liver Disease
by Jung A Eom, Goo Hyun Kwon, Na Yeon Kim, Eun Ju Park, Sung Min Won, Jin Ju Jeong, Ganesan Raja, Haripriya Gupta, Yoseph Asmelash Gebru, Satyapriya Sharma, Ye Rin Choi, Hyeong Seop Kim, Sang Jun Yoon, Ji Ye Hyun, Min Kyo Jeong, Hee Jin Park, Byeong Hyun Min, Mi Ran Choi, Dong Joon Kim and Ki Tae Suk
Int. J. Mol. Sci. 2021, 22(12), 6326; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126326 - 13 Jun 2021
Cited by 9 | Viewed by 3923
Abstract
The gut microbiota has been known to modulate the immune responses in chronic liver diseases. Recent evidence suggests that effects of dietary foods on health care and human diseases are related to both the immune reaction and the microbiome. The gut-microbiome and intestinal [...] Read more.
The gut microbiota has been known to modulate the immune responses in chronic liver diseases. Recent evidence suggests that effects of dietary foods on health care and human diseases are related to both the immune reaction and the microbiome. The gut-microbiome and intestinal immune system play a central role in the control of bacterial translocation-induced liver disease. Dysbiosis, small intestinal bacterial overgrowth, translocation, endotoxemia, and the direct effects of metabolites are the main events in the gut-liver axis, and immune responses act on every pathways of chronic liver disease. Microbiome-derived metabolites or bacteria themselves regulate immune cell functions such as recognition or activation of receptors, the control of gene expression by epigenetic change, activation of immune cells, and the integration of cellular metabolism. Here, we reviewed recent reports about the immunologic role of gut microbiotas in liver disease, highlighting the role of diet in chronic liver disease. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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Graphical abstract

13 pages, 1734 KiB  
Review
Gut Susceptibility to Viral Invasion: Contributing Roles of Diet, Microbiota and Enteric Nervous System to Mucosal Barrier Preservation
by Marcela Julio-Pieper, Alejandra López-Aguilera, Johana Eyzaguirre-Velásquez, Loreto Olavarría-Ramírez, Claudia Ibacache-Quiroga, Javier A. Bravo and Gonzalo Cruz
Int. J. Mol. Sci. 2021, 22(9), 4734; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094734 - 29 Apr 2021
Cited by 9 | Viewed by 3758
Abstract
The gastrointestinal lumen is a rich source of eukaryotic and prokaryotic viruses which, together with bacteria, fungi and other microorganisms comprise the gut microbiota. Pathogenic viruses inhabiting this niche have the potential to induce local as well as systemic complications; among them, the [...] Read more.
The gastrointestinal lumen is a rich source of eukaryotic and prokaryotic viruses which, together with bacteria, fungi and other microorganisms comprise the gut microbiota. Pathogenic viruses inhabiting this niche have the potential to induce local as well as systemic complications; among them, the viral ability to disrupt the mucosal barrier is one mechanism associated with the promotion of diarrhea and tissue invasion. This review gathers recent evidence showing the contributing effects of diet, gut microbiota and the enteric nervous system to either support or impair the mucosal barrier in the context of viral attack. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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18 pages, 510 KiB  
Review
Dietary Influences on the Microbiota–Gut–Brain Axis
by Thomas M. Barber, Georgios Valsamakis, George Mastorakos, Petra Hanson, Ioannis Kyrou, Harpal S. Randeva and Martin O. Weickert
Int. J. Mol. Sci. 2021, 22(7), 3502; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073502 - 28 Mar 2021
Cited by 32 | Viewed by 6560
Abstract
Over unimaginable expanses of evolutionary time, our gut microbiota have co-evolved with us, creating a symbiotic relationship in which each is utterly dependent upon the other. Far from confined to the recesses of the alimentary tract, our gut microbiota engage in complex and [...] Read more.
Over unimaginable expanses of evolutionary time, our gut microbiota have co-evolved with us, creating a symbiotic relationship in which each is utterly dependent upon the other. Far from confined to the recesses of the alimentary tract, our gut microbiota engage in complex and bi-directional communication with their host, which have far-reaching implications for overall health, wellbeing and normal physiological functioning. Amongst such communication streams, the microbiota–gut–brain axis predominates. Numerous complex mechanisms involve direct effects of the microbiota, or indirect effects through the release and absorption of the metabolic by-products of the gut microbiota. Proposed mechanisms implicate mitochondrial function, the hypothalamus–pituitary–adrenal axis, and autonomic, neuro-humeral, entero-endocrine and immunomodulatory pathways. Furthermore, dietary composition influences the relative abundance of gut microbiota species. Recent human-based data reveal that dietary effects on the gut microbiota can occur rapidly, and that our gut microbiota reflect our diet at any given time, although much inter-individual variation pertains. Although most studies on the effects of dietary macronutrients on the gut microbiota report on associations with relative changes in the abundance of particular species of bacteria, in broad terms, our modern-day animal-based Westernized diets are relatively high in fats and proteins and impoverished in fibres. This creates a perfect storm within the gut in which dysbiosis promotes localized inflammation, enhanced gut wall permeability, increased production of lipopolysaccharides, chronic endotoxemia and a resultant low-grade systemic inflammatory milieu, a harbinger of metabolic dysfunction and many modern-day chronic illnesses. Research should further focus on the colony effects of the gut microbiota on health and wellbeing, and dysbiotic effects on pathogenic pathways. Finally, we should revise our view of the gut microbiota from that of a seething mass of microbes to one of organ-status, on which our health and wellbeing utterly depends. Future guidelines on lifestyle strategies for wellbeing should integrate advice on the optimal establishment and maintenance of a healthy gut microbiota through dietary and other means. Although we are what we eat, perhaps more importantly, we are what our gut microbiota thrive on and they thrive on what we eat. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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18 pages, 1110 KiB  
Review
Digestive Inflammation: Role of Proteolytic Dysregulation
by Vincent Mariaule, Aicha Kriaa, Souha Soussou, Soufien Rhimi, Houda Boudaya, Juan Hernandez, Emmanuelle Maguin, Adam Lesner and Moez Rhimi
Int. J. Mol. Sci. 2021, 22(6), 2817; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22062817 - 10 Mar 2021
Cited by 10 | Viewed by 3465
Abstract
Dysregulation of the proteolytic balance is often associated with diseases. Serine proteases and matrix metalloproteases are involved in a multitude of biological processes and notably in the inflammatory response. Within the framework of digestive inflammation, several studies have stressed the role of serine [...] Read more.
Dysregulation of the proteolytic balance is often associated with diseases. Serine proteases and matrix metalloproteases are involved in a multitude of biological processes and notably in the inflammatory response. Within the framework of digestive inflammation, several studies have stressed the role of serine proteases and matrix metalloproteases (MMPs) as key actors in its pathogenesis and pointed to the unbalance between these proteases and their respective inhibitors. Substantial efforts have been made in developing new inhibitors, some of which have reached clinical trial phases, notwithstanding that unwanted side effects remain a major issue. However, studies on the proteolytic imbalance and inhibitors conception are directed toward host serine/MMPs proteases revealing a hitherto overlooked factor, the potential contribution of their bacterial counterpart. In this review, we highlight the role of proteolytic imbalance in human digestive inflammation focusing on serine proteases and MMPs and their respective inhibitors considering both host and bacterial origin. Full article
(This article belongs to the Special Issue Diet-Microbiota and Host Interactions in Intestinal Health and Inflammation)
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