Impact of Microbiome Community Changes on Host Health through Metabolic Dysregulation

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Microbiology and Ecological Metabolomics".

Deadline for manuscript submissions: closed (15 March 2024) | Viewed by 3186

Special Issue Editors

Toyota Technological Institute at Chicago, Chicago, IL 60637, USA
Interests: metagenomics; metabolomics; gut microbiome; immunology; multiomics data integration; machine learning; metabolic dis-ease; autoimmune disease
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60607, USA
Interests: diabetes (both type 1 and 2); gut microbiome; GPCRs; diet and nutrition
Richard and Loan Hill Department of Biomedical Engineering, Computational Functional Genomics Laboratory, University of Illinois at Chicago, Chicago, IL 60607, USA
Interests: computational functional genomics; biostatistics; machine learning; bioengineering and bioinformatics

Special Issue Information

Dear Colleagues,

The human microbiome is a complex ecosystem of microorganisms that inhabit our bodies. Studies in the field of metabolomics have provided new insights into the interactions between the microbiome and its host, highlighting the role these microorganisms play in human health and disease. Research on the microbiome is ongoing and encompasses a wide range of topics, including potential connections between the microbiome and the development of chronic diseases as well as the ways in which the microbiome may influence normal metabolic processes. The microbiome represents a rapidly developing field of study with potential implications for medicine.

This Special Issue is dedicated to exploring the frontiers of microbiome–metabolome interactions and their impact on human health. We welcome submissions that delve into the mechanisms of metabolic dysregulation associated with alterations in the microbiome community and investigate the challenges of integrating clinical microbiome and metabolomic data.

Through this Special Issue, we aim to present current research on the human microbiome and its impact on human health in addition to introducing new computational methods that may aid in our understanding of the microbiome. This is an opportunity to contribute new discoveries, methods, and insights related to the field of the microbiome, metabolomics, and its potential effects on human health.

Dr. Derek Reiman
Dr. Medha Priyadarshini
Prof. Dr. Yang Dai
Guest Editors

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. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • microbiome
  • metabolomics
  • microbial metabolism
  • host–microbe interactions
  • metabolic dysregulation
  • disease
  • host health
  • multiomics data integration

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

23 pages, 11632 KiB  
Article
Conditional Vitamin D Receptor Deletion Induces Fungal and Archaeal Dysbiosis and Altered Metabolites
by Duncan J. Claypool, Yong-Guo Zhang, Yinglin Xia and Jun Sun
Metabolites 2024, 14(1), 32; https://doi.org/10.3390/metabo14010032 - 01 Jan 2024
Viewed by 1347
Abstract
A vitamin D receptor (VDR) deficiency leads to the dysbiosis of intestinal bacteria and is associated with various diseases, including cancer, infections, and inflammatory bowel disease. However, the impact of a VDR deficiency on fungi and archaea is unknown. We conditionally deleted the [...] Read more.
A vitamin D receptor (VDR) deficiency leads to the dysbiosis of intestinal bacteria and is associated with various diseases, including cancer, infections, and inflammatory bowel disease. However, the impact of a VDR deficiency on fungi and archaea is unknown. We conditionally deleted the VDR in Paneth cells (VDRΔPC), intestinal epithelial cells (VDRΔIEC), or myeloid cells (VDRΔLyz) in mice and collected feces for shotgun metagenomic sequencing and untargeted metabolomics. We found that fungi were significantly altered in each knockout (KO) group compared to the VDRLoxp control. The VDRΔLyz mice had the most altered fungi species (three depleted and seven enriched), followed by the VDRΔPC mice (six depleted and two enriched), and the VDRΔIEC mice (one depleted and one enriched). The methanogen Methanofollis liminatans was enriched in the VDRΔPC and VDRΔLyz mice and two further archaeal species (Thermococcus piezophilus and Sulfolobus acidocaldarius) were enriched in the VDRΔLyz mice compared to the Loxp group. Significant correlations existed among altered fungi, archaea, bacteria, and viruses in the KO mice. Functional metagenomics showed changes in several biologic functions, including decreased sulfate reduction and increased biosynthesis of cobalamin (vitamin B12) in VDRΔLyz mice relative to VDRLoxp mice. Fecal metabolites were analyzed to examine the involvement of sulfate reduction and other pathways. In conclusion, a VDR deficiency caused the formation of altered fungi and archaea in a tissue- and sex-dependent manner. These results provide a foundation about the impact of a host factor (e.g., VDR deficiency) on fungi and archaea. It opens the door for further studies to determine how mycobiome and cross-kingdom interactions in the microbiome community and metabolites contribute to the risk of certain diseases. Full article
Show Figures

Figure 1

16 pages, 3418 KiB  
Article
Induction of AHR Signaling in Response to the Indolimine Class of Microbial Stress Metabolites
by Dhwani Patel, Iain A. Murray, Fangcong Dong, Andrew J. Annalora, Krishne Gowda, Denise M. Coslo, Jacek Krzeminski, Imhoi Koo, Fuhua Hao, Shantu G. Amin, Craig B. Marcus, Andrew D. Patterson and Gary H. Perdew
Metabolites 2023, 13(9), 985; https://doi.org/10.3390/metabo13090985 - 31 Aug 2023
Viewed by 1241
Abstract
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that plays an important role in gastrointestinal barrier function, tumorigenesis, and is an emerging drug target. The resident microbiota is capable of metabolizing tryptophan to metabolites that are AHR ligands (e.g., indole-3-acetate). Recently, [...] Read more.
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that plays an important role in gastrointestinal barrier function, tumorigenesis, and is an emerging drug target. The resident microbiota is capable of metabolizing tryptophan to metabolites that are AHR ligands (e.g., indole-3-acetate). Recently, a novel set of mutagenic tryptophan metabolites named indolimines have been identified that are produced by M. morganii in the gastrointestinal tract. Here, we determined that indolimine-200, -214, and -248 are direct AHR ligands that can induce Cyp1a1 transcription and subsequent CYP1A1 enzymatic activity capable of metabolizing the carcinogen benzo(a)pyrene in microsomal assays. In addition, indolimines enhance IL6 expression in a colonic tumor cell line in combination with cytokine treatment. The concentration of indolimine-248 that induces AHR transcriptional activity failed to increase DNA damage. These observations reveal an additional aspect of how indolimines may alter colonic tumorigenesis beyond mutagenic activity. Full article
Show Figures

Figure 1

Back to TopTop