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Cells
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Gut Microbiota in Intestinal Homeostasis
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Gut Microbiota in Intestinal Homeostasis

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 10481

Special Issue Editor

Dr. Parag Kundu

E-Mail Website
Guest Editor
Institute Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China
Interests: microbiota; intestinal epithelium; stem cells; gut-brain axis; colorectal cancer

Special Issue Information

Dear Colleagues,

The gastrointestinal epithelium is a hotspot for communication between the host and its indigenous microbiota. This complex interaction between the microbial communities and a plethora of epithelial cells in the gut is critical as it determines homeostasis or disease outcome. Gut homeostasis represents a state where host functions that control microbial populations and diversity are normal and microbial cues that regulate host physiology are optimally sustained. Although tightly controlled, this bidirectional communication between the host and its microbiome is influenced by multiple extrinsic or intrinsic factors such as diet, environment, seasons, health status, age, and so on.

This Special Issue seeks to explore the intercommunications between the host and its indigenous microbiota that regulate homeostasis, the key players that influence such interactions, and the underlying molecular mechanisms.

Dr. Parag Kundu
Guest Editor

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. Cells 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 2700 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 microbiota
  • homeostasis
  • intestinal epithelium
  • dysbiosis

Published Papers (3 papers)

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Research

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18 pages, 7336 KiB  
Article
Low Gut Microbial Diversity Augments Estrogen-Driven Pulmonary Fibrosis in Female-Predominant Interstitial Lung Disease
by Ozioma S. Chioma, Elizabeth Mallott, Binal Shah-Gandhi, ZaDarreyal Wiggins, Madison Langford, Andrew William Lancaster, Alexander Gelbard, Hongmei Wu, Joyce E. Johnson, Lisa Lancaster, Erin M. Wilfong, Leslie J. Crofford, Courtney G. Montgomery, Luc Van Kaer, Seth Bordenstein, Dawn C. Newcomb and Wonder Puryear Drake
Cells 2023, 12(5), 766; https://doi.org/10.3390/cells12050766 - 28 Feb 2023
Cited by 1 | Viewed by 2756
Abstract
Although profibrotic cytokines, such as IL-17A and TGF-β1, have been implicated in the pathogenesis of interstitial lung disease (ILD), the interactions between gut dysbiosis, gonadotrophic hormones and molecular mediators of profibrotic cytokine expression, such as the phosphorylation of STAT3, have not been defined. [...] Read more.
Although profibrotic cytokines, such as IL-17A and TGF-β1, have been implicated in the pathogenesis of interstitial lung disease (ILD), the interactions between gut dysbiosis, gonadotrophic hormones and molecular mediators of profibrotic cytokine expression, such as the phosphorylation of STAT3, have not been defined. Here, through chromatin immunoprecipitation sequencing (ChIP-seq) analysis of primary human CD4+ T cells, we show that regions within the STAT3 locus are significantly enriched for binding by the transcription factor estrogen receptor alpha (ERa). Using the murine model of bleomycin-induced pulmonary fibrosis, we found significantly increased regulatory T cells compared to Th17 cells in the female lung. The genetic absence of ESR1 or ovariectomy in mice significantly increased pSTAT3 and IL-17A expression in pulmonary CD4+ T cells, which was reduced after the repletion of female hormones. Remarkably, there was no significant reduction in lung fibrosis under either condition, suggesting that factors outside of ovarian hormones also contribute. An assessment of lung fibrosis among menstruating females in different rearing environments revealed that environments favoring gut dysbiosis augment fibrosis. Furthermore, hormone repletion following ovariectomy further augmented lung fibrosis, suggesting pathologic interactions between gonadal hormones and gut microbiota in relation to lung fibrosis severity. An analysis of female sarcoidosis patients revealed a significant reduction in pSTAT3 and IL-17A levels and a concomitant increase in TGF-β1 levels in CD4+ T cells compared to male sarcoidosis patients. These studies reveal that estrogen is profibrotic in females and that gut dysbiosis in menstruating females augments lung fibrosis severity, supporting a critical interaction between gonadal hormones and gut flora in lung fibrosis pathogenesis. Full article
(This article belongs to the Special Issue Gut Microbiota in Intestinal Homeostasis)
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Review

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25 pages, 1580 KiB  
Review
Border Control: The Role of the Microbiome in Regulating Epithelial Barrier Function
by Fernanda Schreiber, Iulia Balas, Matthew J. Robinson and Ghaith Bakdash
Cells 2024, 13(6), 477; https://doi.org/10.3390/cells13060477 - 8 Mar 2024
Cited by 1 | Viewed by 2213
Abstract
The gut mucosal epithelium is one of the largest organs in the body and plays a critical role in regulating the crosstalk between the resident microbiome and the host. To this effect, the tight control of what is permitted through this barrier is [...] Read more.
The gut mucosal epithelium is one of the largest organs in the body and plays a critical role in regulating the crosstalk between the resident microbiome and the host. To this effect, the tight control of what is permitted through this barrier is of high importance. There should be restricted passage of harmful microorganisms and antigens while at the same time allowing the absorption of nutrients and water. An increased gut permeability, or “leaky gut”, has been associated with a variety of diseases ranging from infections, metabolic diseases, and inflammatory and autoimmune diseases to neurological conditions. Several factors can affect gut permeability, including cytokines, dietary components, and the gut microbiome. Here, we discuss how the gut microbiome impacts the permeability of the gut epithelial barrier and how this can be harnessed for therapeutic purposes. Full article
(This article belongs to the Special Issue Gut Microbiota in Intestinal Homeostasis)
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Other

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11 pages, 613 KiB  
Perspective
Interaction between Gut Microbiota and Celiac Disease: From Pathogenesis to Treatment
by Roberta Elisa Rossi, Giulia Dispinzieri, Alessandra Elvevi and Sara Massironi
Cells 2023, 12(6), 823; https://doi.org/10.3390/cells12060823 - 7 Mar 2023
Cited by 9 | Viewed by 5057
Abstract
Celiac disease (CD) is a common systemic disorder that results from an abnormal response of human immunity to gluten intake, affecting the small intestine. In individuals who carry a genetic susceptibility, CD is triggered by environmental factors, including viral infections and dysbiosis of [...] Read more.
Celiac disease (CD) is a common systemic disorder that results from an abnormal response of human immunity to gluten intake, affecting the small intestine. In individuals who carry a genetic susceptibility, CD is triggered by environmental factors, including viral infections and dysbiosis of the gut microbiota. The gut microbiome is essential in controlling the immune system, and recent findings indicate that changes in the gut microbiome may contribute to various chronic immune disorders, such as CD through mechanisms that still require further exploration. Some bacteria exhibit epitopes that mimic gliadin and may enhance an immune response in the host. Other bacteria, including Pseudomonas aeruginosa, may work in conjunction with gluten to trigger and escalate intestinal inflammation. The microbiota may also directly influence antigen development through the production of immunogenic or tolerogenic gluten peptides or directly influence intestinal permeability through the release of zonulin. Finally, the gut microbiome can impact intestinal inflammation by generating proinflammatory or anti-inflammatory cytokines and metabolites. It is crucial to consider the impact of genetic factors (specifically, HLA-DQ haplotypes), perinatal elements such as birth mode, type of infant feeding, and antibiotic and infection exposure on the composition of the early intestinal microbiome. According to the available studies, the gut microbiome alterations associated with CD tend to exhibit a decreased presence of beneficial bacteria, including some anti-inflammatory Bifidobacterium species. However, some controversy remains as some reports have found no significant differences between the gut microbiomes of individuals with and without CD. A better understanding of the gut microbiome’s role in the development of CD would greatly benefit both prevention and treatment efforts, especially in complicated or treatment-resistant cases. Here, we have attempted to summarize the available evidence on the relationship between the gut microbiota and CD, with a particular focus on potential therapeutic targets. Full article
(This article belongs to the Special Issue Gut Microbiota in Intestinal Homeostasis)
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