Gut Microbiome and Metagenome

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Microbial Genetics and Genomics".

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 2131

Special Issue Editors


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Guest Editor
Department of Microbiology, Quaid-i-Azam University, Islamabad 4532, Pakistan
Interests: food; gut microbiome; microbial diversity; nutrition; metabolic diseases; metagenomics; liposome

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Guest Editor
School of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, China
Interests: pan-genome; metagenome; evolution
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Special Issue Information

Dear Colleagues,

Gut microbial communities play a vital role in protecting their hosts against pathogens, regulating immunity, controlling metabolic processes, and are even regarded as a second endocrine organ. However, conventional culture techniques are restricted to the detection of entire microbes of any microbial system. Metagenomic sequencing has achieved progressive development in the investigation of the human gastrointestinal microbiome. Metagenomics can be utilized to explore intestinal microbiome diversity and dysbiosis, as well as its relationship with health and disease. Furthermore, functional metagenomics can discover new functional genes, microbial pathways, antibiotic resistance genes, functional dysbiosis of the intestinal microbiome, and establish connections and co-development between microbiota and host. In this Special Issue of Genes, we would like to convey our current understanding of the human gut microbiome by showcasing some of the best research from around the world. We welcome reviews and original articles in the area of the human gut microbiome.

Prof. Dr. Muhammad Imran
Prof. Dr. Kang Ning
Guest Editors

Manuscript Submission Information

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Keywords

  • gut microbiome
  • microbial diversity
  • microbiome dysbiosis
  • microbiota modulation
  • metagenome

Published Papers (1 paper)

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Research

15 pages, 3154 KiB  
Article
Behavioral and Cognitive Performance Following Exposure to Second-Hand Smoke (SHS) from Tobacco Products Associated with Oxidative-Stress-Induced DNA Damage and Repair and Disruption of the Gut Microbiome
by Jacob Raber, Keaton Stagaman, Kristin D. Kasschau, Conor Davenport, Leilani Lopes, Dennis Nguyen, Eileen Ruth Torres, Thomas J. Sharpton and Glen Kisby
Genes 2023, 14(9), 1702; https://doi.org/10.3390/genes14091702 - 27 Aug 2023
Viewed by 1365
Abstract
Exposure to second-hand Smoke (SHS) remains prevalent. The underlying mechanisms of how SHS affects the brain require elucidation. We tested the hypothesis that SHS inhalation drives changes in the gut microbiome, impacting behavioral and cognitive performance as well as neuropathology in two-month-old wild-type [...] Read more.
Exposure to second-hand Smoke (SHS) remains prevalent. The underlying mechanisms of how SHS affects the brain require elucidation. We tested the hypothesis that SHS inhalation drives changes in the gut microbiome, impacting behavioral and cognitive performance as well as neuropathology in two-month-old wild-type (WT) mice and mice expressing wild-type human tau, a genetic model pertinent to Alzheimer’s disease mice, following chronic SHS exposure (10 months to ~30 mg/m3). SHS exposure impacted the composition of the gut microbiome as well as the biodiversity and evenness of the gut microbiome in a sex-dependent fashion. This variation in the composition and biodiversity of the gut microbiome is also associated with several measures of cognitive performance. These results support the hypothesis that the gut microbiome contributes to the effect of SHS exposure on cognition. The percentage of 8-OHdG-labeled cells in the CA1 region of the hippocampus was also associated with performance in the novel object recognition test, consistent with urine and serum levels of 8-OHdG serving as a biomarker of cognitive performance in humans. We also assessed the effects of SHS on the percentage of p21-labeled cells, an early cellular marker of senescence that is upregulated in bronchial cells after exposure to cigarette smoke. Nuclear staining of p21-labeled cells was more prominent in larger cells of the prefrontal cortex and CA1 hippocampal neurons of SHS-exposed mice than in sham-exposed mice, and there was a significantly greater percentage of labelled cells in the prefrontal cortex and CA1 region of the hippocampus of SHS than air-exposed mice, suggesting that exposure to SHS may result in accelerated brain aging through oxidative-stress-induced injury. Full article
(This article belongs to the Special Issue Gut Microbiome and Metagenome)
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