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Nutrients
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Dietary Effects on Gastrointestinal Microbiota and Health
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Dietary Effects on Gastrointestinal Microbiota and Health

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Prebiotics and Probiotics".

Deadline for manuscript submissions: 15 February 2025 | Viewed by 2207

Special Issue Editors

Dr. João Felipe Mota

E-Mail Website
Guest Editor
School of Nutrition, Federal University of Goiás, Goiânia 74605-080, Brazil
Interests: gut microbiome; nutrition; diet intervention; probiotic; prebiotic; metabolic syndrome; inflammation
Prof. Dr. Christian Hoffmann

E-Mail Website
Guest Editor
School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo 05508-000, Brazil
Interests: gut microbiome; microbial ecology; nutrition; populations; dietary patterns; host-microbiome interaction; immune function
Prof. Dr. Evandro Leite de Souza

E-Mail Website
Guest Editor
Department of Nutrition, Federal University of Paraíba, João Pessoa 58051-900, PB, Brazil
Interests: gut microbiota; probiotics; prebiotics; synbiotics; phenolic compounds; nutraceuticals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue seeks to delve into the intricate relationship between dietary habits and their effects on gastrointestinal (GI) microbiota composition, metabolic activity, and overall health outcomes. With a growing body of research highlighting the pivotal role of the gut microbiome in human health, understanding how dietary choices shape microbial communities in the GI tract has become an important field of investigation. This Special Issue aims to compile advanced research and insights into various aspects of dietary effects on gut microbiome and health. Contributions may include but are not limited to studies elucidating the mechanisms by which specific dietary components influence microbial diversity, function, and dysbiosis in the gut. Additionally, we welcome reviews and original research articles exploring the implications of altered gut microbiota composition and function for health outcomes such as metabolic disorders, immune functions, gastrointestinal diseases, and mental health.

Dr. João Felipe Mota
Prof. Dr. Christian Hoffmann
Prof. Dr. Evandro Leite de Souza
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. Nutrients is an international peer-reviewed open access semimonthly 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 2900 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

  • gut microbiome
  • health
  • diseases
  • dysbiosis
  • probiotic
  • prebiotic
  • synbiotic
  • dietary fiber
  • phenolic compounds
  • dietary interventions
  • metabolites

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Published Papers (2 papers)

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Research

15 pages, 417 KiB  
Article
A Perspective on the Interaction Between Recurrent Lower Urinary Tract Infections and Irritable Bowel Syndrome
by Florina Ruța, Calin Avram, Elena Mardale, Mirela Pribac, Sara Suciu and Victoria Nyulas
Nutrients 2024, 16(21), 3613; https://doi.org/10.3390/nu16213613 - 24 Oct 2024
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Abstract
Introduction: Given the potential overlap in risk factors associated with both irritable bowel syndrome (IBS) and lower urinary tract infections (LUTIs), we aimed to identify factors that may contribute to the development of both conditions, as well as recurrent lower urinary tract infections [...] Read more.
Introduction: Given the potential overlap in risk factors associated with both irritable bowel syndrome (IBS) and lower urinary tract infections (LUTIs), we aimed to identify factors that may contribute to the development of both conditions, as well as recurrent lower urinary tract infections (RLUTIs). Our research also sought to explore overlapping symptoms and interactions between these two disorders. Materials and Methods: The study included young women with a history of urinary tract infections. Participants were divided into three groups: women with sporadic LUTIs (NRLUTIs), women with recurrent LUTIs (RLUTIs), and women with both a history of urinary infections (NRLUTI or RLUTI) and a diagnosis of IBS. The diagnosis of IBS is primarily clinical, relying on symptoms and the exclusion of other gastrointestinal disorders. Data from intestinal microbiota tests were combined with information on patients’ symptom perception, dietary habits, lifestyle, and knowledge regarding their conditions. Results: Abdominal pain, constipation, insufficient knowledge about antibiotic and probiotic use, and nutritionally unbalanced diets were identified as common factors associated with both LUTI-IBS and RLUTI. Conclusions: Our research identified shared risk factors between LUTI, IBS, and RLUTI, suggesting a pathological interdependence between these conditions. Notably, women with RLUTIs often experience gastrointestinal symptoms such as abdominal pain and constipation after consuming foods known to trigger IBS. This highlights that gut dysbiosis is both a risk factor and a potential consequence of RLUTI. The presence of either condition appears to exacerbate the symptoms of the other, further underscoring the intricate connection between RLUTI and IBS in affected individuals. Full article
(This article belongs to the Special Issue Dietary Effects on Gastrointestinal Microbiota and Health)
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20 pages, 4492 KiB  
Article
Bifidobacterium lactis-Derived Vesicles Attenuate Hippocampal Neuroinflammation by Targeting IL-33 to Regulate FoxO6/P53 Signaling
by Xiaoyu Du, Ming Zhang, Ran Wang, Zhaozhong Zeng, Wen Zhao, Bing Fang, Hanglian Lan, Weilian Hung and Haina Gao
Nutrients 2024, 16(21), 3586; https://doi.org/10.3390/nu16213586 - 22 Oct 2024
Viewed by 723
Abstract
Background: Hippocampal Neuroinflammation (HNF) is a critical driver of cognitive impairment. The lipopolysaccharide (LPS) accumulate amyloid beta (Aβ) and lead to HNF. The Bifidobacterium lactis (BL) 99 have anti-inflammatory ability. However, whether BL99-derived microbiota-derived vesicles (MV) could alleviate LPS-induced HNF remains unclear. Methods: [...] Read more.
Background: Hippocampal Neuroinflammation (HNF) is a critical driver of cognitive impairment. The lipopolysaccharide (LPS) accumulate amyloid beta (Aβ) and lead to HNF. The Bifidobacterium lactis (BL) 99 have anti-inflammatory ability. However, whether BL99-derived microbiota-derived vesicles (MV) could alleviate LPS-induced HNF remains unclear. Methods: To investigate, we used ultrafiltration with ultracentrifuge to extract BL99-derived-MV (BL99-MV). We used hippocampal neuronal HT22 cells (HT22) to establish the LPS-induced HNF model, and explored whether BL99-MV alleviate LPS-induced HNF. Results: The confocal microscopy showed that BL99-MV were taken up by HT22 and reduced the oxidative stress (ROS) level. The PCR showed that BL99-MV up-regulate IL-10 level, and down-regulate TNF-α, IL-1β, and IL-6. Transcriptomic analysis revealed 4127 differentially expressed genes, with 2549 genes upregulated and 1578 genes downregulated in the BL99-MV group compared to the LPS group. Compared to the LPS group, BL99-MV decreased FoxO6, IL-33, P53, and NFκB expression, but increased FoxO1 and Bcl2 expression. The WB showed that BL99-MV modulated NFκB, FoxO6, P53, Caspase9, and Caspase3 protein expression by reducing IL-33 expression in HT22. The findings demonstrated IL-33 as a regulator for FoxO6/P53 signaling. Conclusions: Here, we hypothesized that BL99-MV alleviated LPS-induced HNF to promote HT22 survival and synaptic development by regulating FoxO6/P53 signaling by targeting IL-33. Full article
(This article belongs to the Special Issue Dietary Effects on Gastrointestinal Microbiota and Health)
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