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Diet, Gut Microbiota and Human Health
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Diet, Gut Microbiota and Human Health

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 September 2022) | Viewed by 20518

Special Issue Editor

Dr. Alip Borthakur

E-Mail Website
Guest Editor
Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA
Interests: intestinal epithelial physiology and pathophysiology; gut microbiome; inflammatory bowel disease; obesity; intestinal nutrient transport; gut infection; nutrition in health and disease

Special Issue Information

Dear Colleagues, 

Mounting evidence supports the role of diet in modulating the composition and metabolic activity of the human gut microbiota, which, in turn, can have a tremendous impact on the overall health of the host. This impact can be beneficial or detrimental, depending on the relative abundance of beneficial and harmful species of constituent microbial populations. Emerging elegant studies demonstrating that diet can modulate host–microbe interactions herald a promising future therapeutic approach. However, understanding the mechanisms of the effects of diet in modulating the gut microbiota is important to define novel therapeutic modalities. Most dietary nutrients are absorbed in the upper small intestine. However, there are extremely limited studies focused on the impact of small intestinal microbiota on host health, a topic which should be addressed in future studies.  

The focus of this Special Issue, therefore, is to publish featured articles (review articles, original research articles, communications, commentaries) aimed at (1) elucidating the mechanistic details of the diet–microbiota–host cross-talk occurring in different segments of the gut that ultimately determine the health and/or disease state of the host, compiling published studies on this theme; and (2) critically discussing the thoughts, controversies and research gaps in this field that should be addressed in future research.

Dr. Alip Borthakur
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • gut microbiota
  • probiotics and prebiotics
  • intestinal epithelial cells
  • inflammation
  • infection
  • microbial metabolites
  • nutrient absorption and metabolism
  • epithelial barrier function
  • immunomodulation
  • nutrient sensing and gut hormone secretion

Published Papers (5 papers)

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Research

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13 pages, 2306 KiB  
Article
Responses of Ileal and Fecal Microbiota to Withdrawal of Pancreatic Enzyme Replacement Therapy in a Porcine Model of Exocrine Pancreatic Insufficiency
by Julia Hankel, Anne Mößeler, Clara Berenike Hartung, Silke Rath, Lisa Schulten, Christian Visscher, Josef Kamphues and Marius Vital
Int. J. Mol. Sci. 2022, 23(19), 11700; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911700 - 02 Oct 2022
Cited by 1 | Viewed by 1853
Abstract
Little is known regarding the interplay between microbiota and pancreas functions in humans as investigations are usually limited to distal sites, namely the analyses of fecal samples. The aim of this study was to investigate both ileal and fecal microbiota in response to [...] Read more.
Little is known regarding the interplay between microbiota and pancreas functions in humans as investigations are usually limited to distal sites, namely the analyses of fecal samples. The aim of this study was to investigate both ileal and fecal microbiota in response to pancreatic enzyme replacement therapy (PERT) in a porcine model of exocrine pancreatic insufficiency (EPI). PERT was stopped for ten days in ileo-cecal fistulated minipigs with experimentally induced EPI (n = 8) and ileal digesta as well as fecal samples were obtained before withdrawal, during withdrawal and after the reintroduction of PERT. Profound community changes occurred three days after enzyme omission and were maintained throughout the withdrawal phase. A reduction in α-diversity together with relative abundance changes in several taxa, in particular increases in Bifidobacteria (at both sites) and Lactobacilli (only feces) were observed. Overall, dysbiosis events from the ileum had accumulating effects in distal parts of the gastrointestinal tract with additional alterations occurring only in the colon. Changes were reversible after continuing PERT, and one week later, bacterial communities resembled those at baseline. Our study demonstrates the rapid and profound impacts of enzyme withdrawal in bacterial communities, contributing to our understanding of the interplay between pancreas function and microbiota. Full article
(This article belongs to the Special Issue Diet, Gut Microbiota and Human Health)
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18 pages, 3054 KiB  
Article
Butyrate Prevents Induction of CXCL10 and Non-Canonical IRF9 Expression by Activated Human Intestinal Epithelial Cells via HDAC Inhibition
by Sandra G. P. J. Korsten, Laura Peracic, Luka M. B. van Groeningen, Mara A. P. Diks, Herman Vromans, Johan Garssen and Linette E. M. Willemsen
Int. J. Mol. Sci. 2022, 23(7), 3980; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073980 - 02 Apr 2022
Cited by 11 | Viewed by 2855
Abstract
Non-communicable diseases are increasing and have an underlying low-grade inflammation in common, which may affect gut health. To maintain intestinal homeostasis, unwanted epithelial activation needs to be avoided. This study compared the efficacy of butyrate, propionate and acetate to suppress IFN-γ+/−TNF-α induced intestinal [...] Read more.
Non-communicable diseases are increasing and have an underlying low-grade inflammation in common, which may affect gut health. To maintain intestinal homeostasis, unwanted epithelial activation needs to be avoided. This study compared the efficacy of butyrate, propionate and acetate to suppress IFN-γ+/−TNF-α induced intestinal epithelial activation in association with their HDAC inhibitory capacity, while studying the canonical and non-canonical STAT1 pathway. HT-29 were activated with IFN-γ+/−TNF-α and treated with short chain fatty acids (SCFAs) or histone deacetylase (HDAC) inhibitors. CXCL10 release and protein and mRNA expression of proteins involved in the STAT1 pathway were determined. All SCFAs dose-dependently inhibited CXCL10 release of the cells after activation with IFN-γ or IFN-γ+TNF-α. Butyrate was the most effective, completely preventing CXCL10 induction. Butyrate did not affect phosphorylated STAT1, nor phosphorylated NFκB p65, but inhibited IRF9 and phosphorylated JAK2 protein expression in activated cells. Additionally, butyrate inhibited CXCL10, SOCS1, JAK2 and IRF9 mRNA in activated cells. The effect of butyrate was mimicked by class I HDAC inhibitors and a general HDAC inhibitor Trichostatin A. Butyrate is the most potent inhibitor of CXCL10 release compared to other SCFAs and acts via HDAC inhibition. This causes downregulation of CXCL10, JAK2 and IRF9 genes, resulting in a decreased IRF9 protein expression which inhibits the non-canonical pathway and CXCL10 transcription. Full article
(This article belongs to the Special Issue Diet, Gut Microbiota and Human Health)
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20 pages, 37634 KiB  
Article
Gut Mucosal Microbiome Is Perturbed in Rheumatoid Arthritis Mice and Partly Restored after TDAG8 Deficiency or Suppression by Salicylanilide Derivative
by Ngoc Tuan Nguyen, Wei-Hsin Sun, Tzu-Hsuan Chen, Po-Chun Tsai, Chih-Chen Chen and Shir-Ly Huang
Int. J. Mol. Sci. 2022, 23(7), 3527; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073527 - 24 Mar 2022
Cited by 10 | Viewed by 2419
Abstract
Rheumatoid arthritis (RA), an autoimmune disease, is characterized by chronic joint inflammation and pain. We previously found that the deletion of T-cell death-associated gene 8 (TDAG8) significantly reduces disease severity and pain in RA mice. Whether it is by modulating gut microbiota remains [...] Read more.
Rheumatoid arthritis (RA), an autoimmune disease, is characterized by chronic joint inflammation and pain. We previously found that the deletion of T-cell death-associated gene 8 (TDAG8) significantly reduces disease severity and pain in RA mice. Whether it is by modulating gut microbiota remains unclear. In this study, 64 intestinal samples of feces, cecal content, and cecal mucus from the complete Freund’s adjuvant-induced arthritis mouse models were compared. The α- and β-diversity indices of the microbiome were significantly lower in RA mice. Cecal mucus showed a higher ratio of Firmicutes to Bacteroidetes in RA than healthy mice, suggesting the ratio could serve as an RA indicator. Four core genera, Eubacterium_Ventriosum, Alloprevotella, Rikenella, and Treponema, were reduced in content in both feces and mucus RA samples, and could serve microbial markers representing RA progression. TDAG8 deficiency decreased the abundance of proinflammation-related Eubacterium_Xylanophilum, Clostridia, Ruminococcus, Paraprevotella, and Rikenellaceae, which reduced local mucosal inflammation to relieve RA disease severity and pain. The pharmacological block of the TDAG8 function by a salicylanilide derivative partly restored the RA microbiome to a healthy composition. These findings provide a further understanding of specific bacteria interactions with host gut mucus in the RA model. The modulation by TDAG8 on particular bacteria can facilitate microbiota-based therapy. Full article
(This article belongs to the Special Issue Diet, Gut Microbiota and Human Health)
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Review

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25 pages, 1261 KiB  
Review
Dysbiosis in Inflammatory Bowel Disease: Pathogenic Role and Potential Therapeutic Targets
by Patricia Teixeira Santana, Siane Lopes Bittencourt Rosas, Beatriz Elias Ribeiro, Ygor Marinho and Heitor S. P. de Souza
Int. J. Mol. Sci. 2022, 23(7), 3464; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073464 - 23 Mar 2022
Cited by 71 | Viewed by 6803
Abstract
Microbe–host communication is essential to maintain vital functions of a healthy host, and its disruption has been associated with several diseases, including Crohn’s disease and ulcerative colitis, the two major forms of inflammatory bowel disease (IBD). Although individual members of the intestinal microbiota [...] Read more.
Microbe–host communication is essential to maintain vital functions of a healthy host, and its disruption has been associated with several diseases, including Crohn’s disease and ulcerative colitis, the two major forms of inflammatory bowel disease (IBD). Although individual members of the intestinal microbiota have been associated with experimental IBD, identifying microorganisms that affect disease susceptibility and phenotypes in humans remains a considerable challenge. Currently, the lack of a definition between what is healthy and what is a dysbiotic gut microbiome limits research. Nevertheless, although clear proof-of-concept of causality is still lacking, there is an increasingly evident need to understand the microbial basis of IBD at the microbial strain, genomic, epigenomic, and functional levels and in specific clinical contexts. Recent information on the role of diet and novel environmental risk factors affecting the gut microbiome has direct implications for the immune response that impacts the development of IBD. The complexity of IBD pathogenesis, involving multiple distinct elements, suggests the need for an integrative approach, likely utilizing computational modeling of molecular datasets to identify more specific therapeutic targets. Full article
(This article belongs to the Special Issue Diet, Gut Microbiota and Human Health)
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17 pages, 5241 KiB  
Review
The Effect of Bacterial Infections, Probiotics and Zonulin on Intestinal Barrier Integrity
by Paweł Serek and Monika Oleksy-Wawrzyniak
Int. J. Mol. Sci. 2021, 22(21), 11359; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111359 - 21 Oct 2021
Cited by 28 | Viewed by 5675
Abstract
The intestinal barrier plays an extremely important role in maintaining the immune homeostasis of the gut and the entire body. It is made up of an intricate system of cells, mucus and intestinal microbiota. A complex system of proteins allows the selective permeability [...] Read more.
The intestinal barrier plays an extremely important role in maintaining the immune homeostasis of the gut and the entire body. It is made up of an intricate system of cells, mucus and intestinal microbiota. A complex system of proteins allows the selective permeability of elements that are safe and necessary for the proper nutrition of the body. Disturbances in the tightness of this barrier result in the penetration of toxins and other harmful antigens into the system. Such events lead to various digestive tract dysfunctions, systemic infections, food intolerances and autoimmune diseases. Pathogenic and probiotic bacteria, and the compounds they secrete, undoubtedly affect the properties of the intestinal barrier. The discovery of zonulin, a protein with tight junction regulatory activity in the epithelia, sheds new light on the understanding of the role of the gut barrier in promoting health, as well as the formation of diseases. Coincidentally, there is an increasing number of reports on treatment methods that target gut microbiota, which suggests that the prevention of gut-barrier defects may be a viable approach for improving the condition of COVID-19 patients. Various bacteria–intestinal barrier interactions are the subject of this review, aiming to show the current state of knowledge on this topic and its potential therapeutic applications. Full article
(This article belongs to the Special Issue Diet, Gut Microbiota and Human Health)
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