Gut Microbiota and Inflammatory Bowel Disease

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 2537

Special Issue Editor


E-Mail Website
Guest Editor
Department of Medicine and Surgery, University of Insubria, via H Dunant 5, 21100 Varese, Italy
Interests: microbiota-gut-brain axis; enteric nervous system; gut neuromuscular plasticity; dysbiosis; irritable bowel syndrome (IBS); Inflammatory Bowel Disease (IBD)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There is a general consensus that inflammatory bowel disease (IBD) is strictly related to alterations to the gut microbiota (dysbiosis). Changes in the gut saprophytic microbial composition and load highly impact the immune, neuronal, and endocrine responses in the host, representing a fundamental contributor to IBD pathogenesis. Although a straightforward demonstration of a causative connection between IBD and dysbiosis has not been given yet, in recent years, experimental strategies combining different metabolomic, metagenomic, metatranscriptomic, and proteomic approaches have highlighted the mechanistic contribution of microbes and their metabolites to IBD onset and development. When translating to clinics, however, the majority of clinical investigations are represented by retrospective studies, examining the microbiota composition after the onset of the disease while large-scale, highly controlled prospective clinical studies, allowing us to obtain a more comprehensive understanding of the pathophysiological relevance of the gut microbiota in IBD, are lacking. Indeed, a fundamental but yet unsolved issue concerns the possibility that changes in gut microbial ecology and function and the involvement of specific bacterial species may be considered as predictive for clinical questions relevant to IBD. Since IBD patients are represented by genetically and clinically defined subpopulations with highly specific microbial composition and function, the possibility to evaluate the patients’ microbial profile may represent a predictive clinical tool fostering the basis for a personalized microbiome-based therapy for IBD.

Dr. Cristina Giaroni
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

  • IBD
  • dysbiosis
  • microbiota targeting therapies
  • antibiotics
  • probiotics
  • prebiotics
  • postbiotics
  • fecal microbiota transplantation

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

19 pages, 844 KiB  
Review
Gut Microbiota, Inflammatory Bowel Disease, and Cancer: The Role of Guardians of Innate Immunity
by Vincenzo Giambra, Danilo Pagliari, Pierluigi Rio, Beatrice Totti, Chiara Di Nunzio, Annalisa Bosi, Cristina Giaroni, Antonio Gasbarrini, Giovanni Gambassi and Rossella Cianci
Cells 2023, 12(22), 2654; https://doi.org/10.3390/cells12222654 - 19 Nov 2023
Cited by 4 | Viewed by 2288
Abstract
Inflammatory bowel diseases (IBDs) are characterized by a persistent low-grade inflammation that leads to an increased risk of colorectal cancer (CRC) development. Several factors are implicated in this pathogenetic pathway, such as innate and adaptive immunity, gut microbiota, environment, and xenobiotics. At the [...] Read more.
Inflammatory bowel diseases (IBDs) are characterized by a persistent low-grade inflammation that leads to an increased risk of colorectal cancer (CRC) development. Several factors are implicated in this pathogenetic pathway, such as innate and adaptive immunity, gut microbiota, environment, and xenobiotics. At the gut mucosa level, a complex interplay between the immune system and gut microbiota occurs; a disequilibrium between these two factors leads to an alteration in the gut permeability, called ‘leaky gut’. Subsequently, an activation of several inflammatory pathways and an alteration of gut microbiota composition with a proliferation of pro-inflammatory bacteria, known as ‘pathobionts’, take place, leading to a further increase in inflammation. This narrative review provides an overview on the principal Pattern Recognition Receptors (PRRs), including Toll-like receptors (TLRs) and NOD-like receptors (NLRs), focusing on their recognition mechanisms, signaling pathways, and contributions to immune responses. We also report the genetic polymorphisms of TLRs and dysregulation of NLR signaling pathways that can influence immune regulation and contribute to the development and progression of inflammatory disease and cancer. Full article
(This article belongs to the Special Issue Gut Microbiota and Inflammatory Bowel Disease)
Show Figures

Figure 1

Back to TopTop