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Special Issue Editor

Special Issue Information

Dear Colleagues,

The gut microbiota and their metabolites have been receiving a lot of attention in terms of their regulatory effects on the immune system in the past decade. Major microbial metabolites include the carbohydrate metabolites short-chain fatty acids, amino acid metabolites, and secondary bile acid metabolites. These metabolites function through host-receptor-dependent and independent mechanisms to regulate cells of the innate immune system, which include epithelial cells, NK cells, innate lymphoid cells, dendritic cells, macrophages, and granulocytes. Major host receptors for these microbial metabolites include G protein-coupled receptors (GPR43, GPR41, GPR109A, Olfr78 and TGR5) for fast regulatory actions in the cytoplasm and nuclear receptors (PXR, LXR, VDR, and FXR) and other receptors such as aryl hydrocarbon receptor (AHR) for gene expression regulation in the nucleus. Recent advances indicate that these metabolites regulate innate immunity, host metabolism, inflammation, cancer, tissue repair and even regulation of adaptive immune responses.

Despite the recent advances in this area, I feel that we have only scratched the surface so far of the important functions of these metabolites in the immune system and host physiology. This special issue of Metabolites will be dedicated for publishing current advances on the functions of gut microbial metabolites in regulating the innate immune system, which encompasses not only immune cells but also barrier tissue cells.

Dr. Agnieszka M. Smolinska
Guest Editor

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Keywords

Microbial metabolites
Short-chain fatty acids
Tryptophan metabolites
Secondary bile acid metabolites
Epithelial cells
Dendritic cells
Innate lymphoid cells
NK cells
Macrophages
Inflammation
Infection
Barrier function
Wound repair
Metabolism
Cancer

Published Papers (2 papers)

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Research

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19 pages, 5605 KiB

Open AccessArticle

Flavin-Containing Monooxygenase 3 (FMO3) Is Critical for Dioxin-Induced Reorganization of the Gut Microbiome and Host Insulin Sensitivity

by William Massey, Lucas J. Osborn, Rakhee Banerjee, Anthony Horak, Kevin K. Fung, Danny Orabi, E. Ricky Chan, Naseer Sangwan, Zeneng Wang and J. Mark Brown

Metabolites 2022, 12(4), 364; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo12040364 - 18 Apr 2022

Cited by 5 | Viewed by 3231

Abstract

Exposure to some environmental pollutants can have potent endocrine-disrupting effects, thereby promoting hormone imbalance and cardiometabolic diseases such as non-alcoholic fatty liver disease (NAFLD), diabetes, and cardiorenal diseases. Recent evidence also suggests that many environmental pollutants can reorganize the gut microbiome to potentially impact these diverse human diseases. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is among the most potent endocrine-disrupting dioxin pollutants, yet our understanding of how TCDD impacts the gut microbiome and systemic metabolism is incompletely understood. Here, we show that TCDD exposure in mice profoundly stimulates the hepatic expression of flavin-containing monooxygenase 3 (Fmo3), which is a hepatic xenobiotic metabolizing enzyme that is also responsible for the production of the gut microbiome-associated metabolite trimethylamine N-oxide (TMAO). Interestingly, an enzymatic product of FMO3 (TMAO) has been associated with the same cardiometabolic diseases that these environmental pollutants promote. Therefore, here, we examined TCDD-induced alterations in the gut microbiome, host liver transcriptome, and glucose tolerance in Fmo3^+/+ and Fmo3^−/− mice. Our results show that Fmo3 is a critical component of the transcriptional response to TCDD, impacting the gut microbiome, host liver transcriptome, and systemic glucose tolerance. Collectively, this work uncovers a previously underappreciated role for Fmo3 in integrating diet–pollutant–microbe–host interactions. Full article

(This article belongs to the Special Issue Insights into How Gut Microbial Metabolites Regulate Innate Immune Responses)

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Other

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25 pages, 2241 KiB

Open AccessSystematic Review

Systematic Review: Contribution of the Gut Microbiome to the Volatile Metabolic Fingerprint of Colorectal Neoplasia

by Robert van Vorstenbosch, Hao Ran Cheng, Daisy Jonkers, John Penders, Erik Schoon, Ad Masclee, Frederik-Jan van Schooten, Agnieszka Smolinska and Zlatan Mujagic

Metabolites 2023, 13(1), 55; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo13010055 - 30 Dec 2022

Cited by 8 | Viewed by 1950

Abstract

Colorectal cancer (CRC) has been associated with changes in volatile metabolic profiles in several human biological matrices. This enables its non-invasive detection, but the origin of these volatile organic compounds (VOCs) and their relation to the gut microbiome are not yet fully understood. This systematic review provides an overview of the current understanding of this topic. A systematic search using PubMed, Embase, Medline, Cochrane Library, and the Web of Science according to PRISMA guidelines resulted in seventy-one included studies. In addition, a systematic search was conducted that identified five systematic reviews from which CRC-associated gut microbiota data were extracted. The included studies analyzed VOCs in feces, urine, breath, blood, tissue, and saliva. Eight studies performed microbiota analysis in addition to VOC analysis. The most frequently reported dysregulations over all matrices included short-chain fatty acids, amino acids, proteolytic fermentation products, and products related to the tricarboxylic acid cycle and Warburg metabolism. Many of these dysregulations could be related to the shifts in CRC-associated microbiota, and thus the gut microbiota presumably contributes to the metabolic fingerprint of VOC in CRC. Future research involving VOCs analysis should include simultaneous gut microbiota analysis. Full article

(This article belongs to the Special Issue Insights into How Gut Microbial Metabolites Regulate Innate Immune Responses)

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