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 1758

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 (1 paper)

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Research

18 pages, 4613 KiB  
Article
Integrated Analysis of the Transcriptome and Microbial Diversity in the Intestine of Miniature Pig Obesity Model
by Wenjing Qi, Siran Zhu, Lingli Feng, Jinning Liang, Xiaoping Guo, Feng Cheng, Yafen Guo, Ganqiu Lan and Jing 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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