Intestinal Dysbiosis

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Gut Microbiota".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 3735

Special Issue Editor


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Guest Editor
Section of Clinical Nutrition and Nutrigenomic, Department of Biomedicine and Prevention, University of Tor Vergata, Rome, Italy
Interests: microbiota; microbiome; leaky gut; diet; inflammation; obesity; microbes; bacteria
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Special Issue Information

Dear Colleagues,

The human gut flora is a highly diverse ecosystem of trillions of bacteria that live in our digestive tract and is often referred to as the microbiota or gut flora but is colloquially categorized into "good" or "bad" bacteria. As the name suggests, good bacteria help protect our health while bad bacteria harm us. When the balance between good and bad bacteria is "off balance," it is called a dysbiosis.

Dysbiosis is associated with multiple systemic diseases. For example, an imbalance of intestinal flora can cause irritable bowel syndrome. Imbalances in the gut microbiota contribute to the development or progression of a range of rheumatic diseases; including rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, systemic sclerosis, Sjogren's Syndrome, etc.; by affecting the balance between pro-inflammatory and anti-inflammatory immune responses. Gut flora interacts bidirectionally with the nervous system via the flora–gut–brain axis. At present, the research on gut microbiota is still in its infancy, and there are relatively few studies on causality and mechanisms. This Special Issue welcomes original research articles and review articles related to recent discoveries concerning interactions between intestinal dysbiosis and diseases.

Prof. Dr. Giuseppe Merra
Guest Editor

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Keywords

  • gut flora
  • intestinal flora
  • dysbiosis
  • inflammatory bowel diseases
  • leaky gut

Published Papers (3 papers)

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Research

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11 pages, 7062 KiB  
Article
AG1®, a Novel Synbiotic, Maintains Gut Barrier Function following Inflammatory Challenge in a Caco-2/THP1-Blue™ Co-Culture Model
by Philip A. Sapp, Jeremy R. Townsend, Trevor O. Kirby, Marlies Govaert, Cindy Duysburgh, Lynn Verstrepen, Massimo Marzorati, Tess M. Marshall and Ralph Esposito
Microorganisms 2024, 12(7), 1263; https://doi.org/10.3390/microorganisms12071263 - 21 Jun 2024
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Abstract
Nutritional interventions to reduce gastrointestinal (GI) permeability are of significant interest to physically active adults and those experiencing chronic health conditions. This in vitro study was designed to assess the impact of AG1, a novel synbiotic, on GI permeability following an inflammatory challenge. [...] Read more.
Nutritional interventions to reduce gastrointestinal (GI) permeability are of significant interest to physically active adults and those experiencing chronic health conditions. This in vitro study was designed to assess the impact of AG1, a novel synbiotic, on GI permeability following an inflammatory challenge. Interventions [AG1 (vitamins/minerals, pre-/probiotics, and phytonutrients) and control (control medium)] were fed separately into a human GI tract model (stomach, small intestine, and colon). In the colonic phase, the GI contents were combined with fecal inocula from three healthy human donors. GI permeability was evaluated with transepithelial electrical resistance (TEER) in a Caco-2 (apical)/THP1-Blue™ (basolateral) co-culture model. The apical side received sodium butyrate (positive control) or Caco-2 complete medium (negative control) during baseline testing. In the 24 h experiment, the apical side received colonic simulation isolates from the GI model, and the basolateral side was treated with Caco-2 complete medium, then 6 h treatment with lipopolysaccharide. TEER was assessed at 0 h and 24 h, and inflammatory markers were measured at 30 h in triplicate. Paired samples t-tests were used to evaluate endpoint mean difference (MD) for AG1 vs. control. TEER was higher for AG1 (mean ± SD: 99.89 ± 1.32%) vs. control (mean ± SD: 92.87 ± 1.22%) following activated THP1-induced damage [MD: 7.0% (p < 0.05)]. AG1 maintained TEER similar to the level of the negative control [−0.1% (p = 0.02)]. No differences in inflammatory markers were observed. These in vitro data suggest that acute supplementation with AG1 might stimulate protective effects on GI permeability. These changes may be driven by SCFA production due to the pre-/probiotic properties of AG1, but more research is needed. Full article
(This article belongs to the Special Issue Intestinal Dysbiosis)
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18 pages, 4613 KiB  
Article
Integrated Analysis of the Transcriptome and Microbial Diversity in the Intestine of Miniature Pig Obesity Model
by Wen**g Qi, Siran Zhu, Lingli Feng, **ning Liang, ** Guo, Feng Cheng, Yafen Guo, Ganqiu Lan and **g Liang
Microorganisms 2024, 12(2), 369; https://doi.org/10.3390/microorganisms12020369 - 10 Feb 2024
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Abstract
Obesity, a key contributor to metabolic disorders, necessitates an in-depth understanding of its pathogenesis and prerequisites for prevention. Guangxi Bama miniature pig (GBM) offers an apt model for obesity-related studies. In this research, we used transcriptomics and 16S rRNA gene sequencing to discern [...] Read more.
Obesity, a key contributor to metabolic disorders, necessitates an in-depth understanding of its pathogenesis and prerequisites for prevention. Guangxi Bama miniature pig (GBM) offers an apt model for obesity-related studies. In this research, we used transcriptomics and 16S rRNA gene sequencing to discern the differentially expressed genes (DEGs) within intestinal (jejunum, ileum, and colon) tissues and variations in microbial communities in intestinal contents of GBM subjected to normal diets (ND) and high-fat, high-carbohydrate diets (HFHCD). After a feeding duration of 26 weeks, the HFHCD-fed experimental group demonstrated notable increases in backfat thickness, BMI, abnormal blood glucose metabolism, and blood lipid levels alongside the escalated serum expression of pro-inflammatory factors and a marked decline in intestinal health status when compared to the ND group. Transcriptomic analysis revealed a total of 1669 DEGs, of which 27 had similar differences in three intestinal segments across different groups, including five immune related genes: COL6A6, CYP1A1, EIF2AK2, NMI, and LGALS3B. Further, we found significant changes in the microbiota composition, with a significant decrease in beneficial bacterial populations within the HFHCD group. Finally, the results of integrated analysis of microbial diversity with transcriptomics show a positive link between certain microbial abundance (Solibacillus, norank_f__Saccharimonadaceae, Candidatus_Saccharimonas, and unclassified_f__Butyricicoccaceae) and changes in gene expression (COL6A6 and NMI). Overall, HFHCD appears to co-contribute to the initiation and progression of obesity in GBM by aggravating inflammatory responses, disrupting immune homeostasis, and creating imbalances in intestinal flora. Full article
(This article belongs to the Special Issue Intestinal Dysbiosis)
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Review

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15 pages, 3222 KiB  
Review
The Importance of Maintaining and Improving a Healthy Gut Microbiota in Athletes as a Preventive Strategy to Improve Heat Tolerance and Acclimatization
by Sergi Cinca-Morros and Jesús Álvarez-Herms
Microorganisms 2024, 12(6), 1160; https://doi.org/10.3390/microorganisms12061160 - 6 Jun 2024
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Abstract
Exposure to passive heat (acclimation) and exercise under hot conditions (acclimatization), known as heat acclimation (HA), are methods that athletes include in their routines to promote faster recovery and enhance physiological adaptations and performance under hot conditions. Despite the potential positive effects of [...] Read more.
Exposure to passive heat (acclimation) and exercise under hot conditions (acclimatization), known as heat acclimation (HA), are methods that athletes include in their routines to promote faster recovery and enhance physiological adaptations and performance under hot conditions. Despite the potential positive effects of HA on health and physical performance in the heat, these stimuli can negatively affect gut health, impairing its functionality and contributing to gut dysbiosis. Blood redistribution to active muscles and peripheral vascularization exist during exercise and HA stimulus, promoting intestinal ischemia. Gastrointestinal ischemia can impair intestinal permeability and aggravate systemic endotoxemia in athletes during exercise. Systemic endotoxemia elevates the immune system as an inflammatory responses in athletes, impairing their adaptive capacity to exercise and their HA tolerance. Better gut microbiota health could benefit exercise performance and heat tolerance in athletes. This article suggests that: (1) the intestinal modifications induced by heat stress (HS), leading to dysbiosis and altered intestinal permeability in athletes, can decrease health, and (2) a previously acquired microbial dysbiosis and/or leaky gut condition in the athlete can negatively exacerbate the systemic effects of HA. Maintaining or improving the healthy gut microbiota in athletes can positively regulate the intestinal permeability, reduce endotoxemic levels, and control the systemic inflammatory response. In conclusion, strategies based on positive daily habits (nutrition, probiotics, hydration, chronoregulation, etc.) and preventing microbial dysbiosis can minimize the potentially undesired effects of applying HA, favoring thermotolerance and performance enhancement in athletes. Full article
(This article belongs to the Special Issue Intestinal Dysbiosis)
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