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Gut Dysbiosis: Molecular Mechanisms and Therapies

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 31576

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Special Issue Editors

Dr. Federica Laudisi

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Guest Editor

Department of Systems Medicine, University of Rome “Tor Vergata”, Rome, Italy
Interests: inflammatory bowel disease; intestinal inflammation; colorectal cancer; intestinal epithelial barrier; microbiota; inflammasome
Special Issues, Collections and Topics in MDPI journals

Dr. Carmine Stolfi

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Guest Editor

Department of Systems Medicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
Interests: colorectal cancer; immunotherapy; inflammatory bowel diseases; anti-cancer drugs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Several studies have shown that gut dysbiosis—characterized by a reduction in microbial diversity, decreased frequency of beneficial bacterial strains and overgrowth of pathobionts—frequently associates with the development of intestinal and extra-intestinal disorders (e.g., neurological disorders). Many environmental factors (including diet, drugs and stress) can trigger gut dysbiosis by altering the complex interaction between microbial ecology and the host immune system, thereby promoting intestinal epithelial barrier dysfunctions that may ultimately lead to the development of several pathological conditions. Targeting gut dysbiosis, in combination with standard therapies, is now considered a valuable and promising strategy to prevent and/or treat gut-related diseases, and a better understanding of the molecular and cellular pathways underlying this condition is definitely required.

In this Special Issue, we invite researchers working on gut dysbiosis to submit original articles or reviews to improve our knowledge on this complex and fascinating field.

Potential topics include, but are not limited to, the following:

- Role of dysbiotic microbiota and microbial metabolites in gut homeostasis, intestinal barrier function and host immune system;

- Contribution of gut dysbiosis to the development of intestinal (e.g., inflammatory bowel diseases, colorectal cancer) and extra-intestinal disorders (e.g., neurological disorders, diabetes);

- Therapeutic strategies for gut microbiota modulation in pathological conditions (e.g., probiotic treatment, fecal microbiota transplantation).

You may choose our Joint Special Issue in International Journal of Molecular Sciences.

Dr. Federica Laudisi
Dr. Carmine Stolfi
Guest Editors

Manuscript Submission Information

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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. Biomedicines 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 2600 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.

Related Special Issue

Gut Dysbiosis: Molecular Mechanisms and Therapies 2.0 in Biomedicines (6 articles)

Published Papers (7 papers)

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Research

Jump to: Review

22 pages, 3885 KiB

Open AccessArticle

Antibiotic Treatment during Pregnancy Alters Offspring Gut Microbiota in a Sex-Dependent Manner

by Abdullah M. Madany, Heather K. Hughes and Paul Ashwood

Biomedicines 2022, 10(5), 1042; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10051042 - 30 Apr 2022

Cited by 6 | Viewed by 2802

Abstract

This study investigated the effect of antibiotics administered to pregnant dams on offspring gut microbiome composition and metabolic capabilities, and how these changes in the microbiota may influence their immune responses in both the periphery and the brain. We orally administered a broad-spectrum antibiotic (ABX) cocktail consisting of vancomycin 0.5 mg/mL, ampicillin 1 mg/mL, and neomycin 1 mg/mL to pregnant dams during late gestation through birth. Bacterial DNA was extracted from offspring fecal samples, and 16S ribosomal RNA gene was sequenced by Illumina, followed by analysis of gut microbiota composition and PICRUSt prediction. Serum and brain tissue cytokine levels were analyzed by Luminex. Our results indicate that the ABX-cocktail led to significant diversity and taxonomic changes to the offspring’s gut microbiome. In addition, the predicted KEGG and MetaCyc pathways were significantly altered in the offspring. Finally, there were decreased innate inflammatory cytokines and chemokines and interleukin (IL)-17 seen in the brains of ABX-cocktail offspring in response to lipopolysaccharide (LPS) immune challenge. Our results suggest that maternal ABX can produce long-lasting effects on the gut microbiome and neuroimmune responses of offspring. These findings support the role of the early microbiome in the development of offspring gastrointestinal and immune systems. Full article

(This article belongs to the Special Issue Gut Dysbiosis: Molecular Mechanisms and Therapies)

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18 pages, 3820 KiB

Open AccessArticle

Gut Microbiota-Derived Small Extracellular Vesicles Endorse Memory-like Inflammatory Responses in Murine Neutrophils

by Trim Lajqi, Natascha Köstlin-Gille, Stefan Hillmer, Maylis Braun, Simon A. Kranig, Stefanie Dietz, Christian Krause, Jessica Rühle, David Frommhold, Johannes Pöschl, Christian Gille and Hannes Hudalla

Biomedicines 2022, 10(2), 442; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10020442 - 14 Feb 2022

Cited by 18 | Viewed by 2888

Abstract

Neutrophils are classically characterized as merely reactive innate effector cells. However, the microbiome is known to shape the education and maturation process of neutrophils, improving their function and immune-plasticity. Recent reports demonstrate that murine neutrophils possess the ability to exert adaptive responses after exposure to bacterial components such as LPS (Gram-negative bacteria) or LTA (Gram-positive bacteria). We now ask whether small extracellular vesicles (EVs) from the gut may directly mediate adaptive responses in neutrophils in vitro. Murine bone marrow-derived neutrophils were primed in vitro by small EVs of high purity collected from colon stool samples, followed by a second hit with LPS. We found that low-dose priming with gut microbiota-derived small EVs enhanced pro-inflammatory sensitivity as indicated by elevated levels of TNF-α, IL-6, ROS and MCP-1 and increased migratory and phagocytic activity. In contrast, high-dose priming resulted in a tolerant phenotype, marked by increased IL-10 and decreased transmigration and phagocytosis. Alterations in TLR2/MyD88 as well as TLR4/MyD88 signaling were correlated with the induction of adaptive cues in neutrophils in vitro. Taken together, our study shows that small EVs from stools can drive adaptive responses in neutrophils in vitro and may represent a missing link in the gut–immune axis. Full article

(This article belongs to the Special Issue Gut Dysbiosis: Molecular Mechanisms and Therapies)

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21 pages, 4289 KiB

Open AccessArticle

Clostridium butyricum MIYAIRI 588 Modifies Bacterial Composition under Antibiotic-Induced Dysbiosis for the Activation of Interactions via Lipid Metabolism between the Gut Microbiome and the Host

by Tadashi Ariyoshi, Mao Hagihara, Susumu Tomono, Shuhei Eguchi, Ayaka Minemura, Daiki Miura, Kentaro Oka, Motomichi Takahashi, Yuka Yamagishi and Hiroshige Mikamo

Biomedicines 2021, 9(8), 1065; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9081065 - 22 Aug 2021

Cited by 18 | Viewed by 3752

Abstract

The gut microbiome is closely related to gut metabolic functions, and the gut microbiome and host metabolic functions affect each other. Clostridium butyricum MIYAIRI 588 (CBM 588) upregulates protectin D1 production in host colon tissue following G protein-coupled receptor (GPR) 120 activation to protect gut epithelial cells under antibiotic-induced dysbiosis. However, how CBM 588 enhances polyunsaturated fatty acid (PUFA) metabolites remains unclear. Therefore, we focused on the metabolic function alterations of the gut microbiome after CBM 588 and protectin D1 administration to reveal the interaction between the host and gut microbiome through lipid metabolism during antibiotic-induced dysbiosis. Consequently, CBM 588 modified gut microbiome and increased the butyric acid and oleic acid content. These lipid metabolic modifications induced GPR activation, which is a trigger of ERK 1/2 signaling and directed differentiation of downstream immune cells in the host colon tissue. Moreover, endogenous protectin D1 modified the gut microbiome, similar to CBM 588. This is the first study to report that CBM 588 influences the interrelationship between colon tissue and the gut microbiome through lipid metabolism. These findings provide insights into the mechanisms of prevention and recovery from inflammation and the improvement of host metabolism by CBM 588. Full article

(This article belongs to the Special Issue Gut Dysbiosis: Molecular Mechanisms and Therapies)

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22 pages, 1141 KiB

Open AccessArticle

Involvement of Gut Microbiota in Schizophrenia and Treatment Resistance to Antipsychotics

by Mirko Manchia, Andrea Fontana, Concetta Panebianco, Pasquale Paribello, Carlo Arzedi, Eleonora Cossu, Mario Garzilli, Maria Antonietta Montis, Andrea Mura, Claudia Pisanu, Donatella Congiu, Massimiliano Copetti, Federica Pinna, Valerio Pazienza, Alessio Squassina and Bernardo Carpiniello

Biomedicines 2021, 9(8), 875; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9080875 - 23 Jul 2021

Cited by 20 | Viewed by 3758

Abstract

The gut microbiota is constituted by more than 40,000 bacterial species involved in key processes including high order brain functions. Altered composition of gut microbiota has been implicated in psychiatric disorders and in modulating the efficacy and safety of psychotropic medications. In this work we characterized the composition of the gut microbiota in 38 patients with schizophrenia (SCZ) and 20 healthy controls (HC), and tested if SCZ patients with different response to antipsychotics (18 patients with treatment resistant schizophrenia (TRS), and 20 responders (R)) had specific patterns of gut microbiota composition associated with different response to antipsychotics. Moreover, we also tested if patients treated with typical antipsychotics (n = 20) presented significant differences when compared to patients treated with atypical antipsychotics (n = 31). Our findings showed the presence of distinct composition of gut microbiota in SCZ versus HC, with several bacteria at the different taxonomic levels only present in either one group or the other. Similar findings were observed also depending on treatment response and exposure to diverse classes of antipsychotics. Our results suggest that composition of gut microbiota could constitute a biosignatures of SCZ and TRS. Full article

(This article belongs to the Special Issue Gut Dysbiosis: Molecular Mechanisms and Therapies)

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14 pages, 2511 KiB

Open AccessArticle

Microbiota Depletion Promotes Human Rotavirus Replication in an Adult Mouse Model

by Roberto Gozalbo-Rovira, Cristina Santiso-Bellón, Javier Buesa, Antonio Rubio-del-Campo, Susana Vila-Vicent, Carlos Muñoz, María J. Yebra, Vicente Monedero and Jesús Rodríguez-Díaz

Biomedicines 2021, 9(7), 846; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9070846 - 20 Jul 2021

Cited by 5 | Viewed by 2933

Abstract

Intestinal microbiota-virus-host interaction has emerged as a key factor in mediating enteric virus pathogenicity. With the aim of analyzing whether human gut bacteria improve the inefficient replication of human rotavirus in mice, we performed fecal microbiota transplant (FMT) with healthy infants as donors in antibiotic-treated mice. We showed that a simple antibiotic treatment, irrespective of FMT, resulted in viral shedding for 6 days after challenge with the human rotavirus G1P[8] genotype Wa strain (RVwa). Rotavirus titers in feces were also significantly higher in antibiotic-treated animals with or without FMT but they were decreased in animals subject to self-FMT, where a partial re-establishment of specific bacterial taxons was evidenced. Microbial composition analysis revealed profound changes in the intestinal microbiota of antibiotic-treated animals, whereas some bacterial groups, including members of Lactobacillus, Bilophila, Mucispirillum, and Oscillospira, recovered after self-FMT. In antibiotic-treated and FMT animals where the virus replicated more efficiently, differences were observed in gene expression of immune mediators, such as IL1β and CXCL15, as well as in the fucosyltransferase FUT2, responsible for H-type antigen synthesis in the small intestine. Collectively, our results suggest that antibiotic-induced microbiota depletion eradicates the microbial taxa that restrict human rotavirus infectivity in mice. Full article

(This article belongs to the Special Issue Gut Dysbiosis: Molecular Mechanisms and Therapies)

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Review

Jump to: Research

27 pages, 2084 KiB

Open AccessEditor’s ChoiceReview

Implication of Intestinal Barrier Dysfunction in Gut Dysbiosis and Diseases

by Carmine Stolfi, Claudia Maresca, Giovanni Monteleone and Federica Laudisi

Biomedicines 2022, 10(2), 289; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10020289 - 27 Jan 2022

Cited by 78 | Viewed by 10716

Abstract

The intestinal mucosal barrier, also referred to as intestinal barrier, is widely recognized as a critical player in gut homeostasis maintenance as it ensures the complex crosstalk between gut microbes (both commensals and pathogens) and the host immune system. Highly specialized epithelial cells constantly cope with several protective and harmful agents to maintain the multiple physiological functions of the barrier as well as its integrity. However, both genetic defects and environmental factors can break such equilibrium, thus promoting gut dysbiosis, dysregulated immune-inflammatory responses, and even the development of chronic pathological conditions. Here, we review and discuss the molecular and cellular pathways underlying intestinal barrier structural and functional homeostasis, focusing on potential alterations that may undermine this fine balance. Full article

(This article belongs to the Special Issue Gut Dysbiosis: Molecular Mechanisms and Therapies)

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18 pages, 693 KiB

Open AccessReview

Gastric Microbiota beyond H. pylori: An Emerging Critical Character in Gastric Carcinogenesis

by Jun Wen, Harry Cheuk-Hay Lau, Maikel Peppelenbosch and Jun Yu

Biomedicines 2021, 9(11), 1680; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9111680 - 12 Nov 2021

Cited by 11 | Viewed by 3000

Abstract

Gastric cancer (GC) is one of the global leading causes of cancer death. The association between Helicobacter pylori, which is a predominant risk factor for GC, with GC development has been well-studied. Recently, accumulating evidence has demonstrated the presence of a large population of microorganisms other than H. pylori in the human stomach. Existing sequencing studies have revealed microbial compositional and functional alterations in patients with GC and highlighted a progressive shift in the gastric microbiota in gastric carcinogenesis with marked enrichments of oral or intestinal commensals. Moreover, using a combination of gastric bacterial signatures, GC patients could be significantly distinguished from patients with gastritis. These findings, therefore, emphasize the importance of a collective microbial community in gastric carcinogenesis. Here, we provide an overview of non-H. pylori gastric microbes in gastric carcinogenesis. The molecular mechanisms of gastric microbes-related carcinogenesis and potential clinical applications of gastric microbiota as biomarkers of GC are also explored. Full article

(This article belongs to the Special Issue Gut Dysbiosis: Molecular Mechanisms and Therapies)

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