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Molecular Research on Inflammatory Diseases of the Gut in Humans and Animals

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 May 2025 | Viewed by 2258

Special Issue Editor


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Guest Editor
Department of Biotechnology, School of Applied Biology and Biotechnology, Agricultural University of Athens, 75 Iera Odos St., 11855 Athens, Greece
Interests: inflammatory bowel disease; Crohn’s disease; ulcerative colitis; Johne’s disease; gene regulation; biomarker

Special Issue Information

Dear Colleagues,

The digestive system development and gastrointestinal tract cell functions are ruled and determined by a multifaceted regime of genetic and epigenetic regulators, influenced by the environment during development. There is a genetic component in many gastrointestinal (GI) diseases (e.g., inflammatory bowel disease—IBD) in which conditions are inherited, and “marked” with epigenetic “signatures” under a given environment. Importantly, among the environmental challenges, the significant role of microbial intestine flora has been acknowledged in all aspects of pathobiology of the GI tract, for signs of malfunction from benign disease to malignancy.

The complex interactions that regulate mucosa immunity, GI homeostasis, normal intestine barrier function, defense against infections, macrophage/T-cell responses, and other associated mechanisms constitute not only a sophisticated immune system to protect the GI from infection, inflammation, and dysfunction, but also include a multidimensional network of molecular components that control normal cell function. Thus, either intestinal barrier dysfunction and inappropriate immune activation in IBD-related pathologies or infectious disease, namely Johne’s disease (or paratuberculosis), are considered debilitating diseases of the GI with high risk of morbidity in humans and animals, respectively. The genetic basis of complex symptom-based disorders, including symptoms from the gastrointestinal tract, is not fully understood in humans and animals. Beyond the anticipated, but inconclusive, zoonotic risk that infectious agents entail in these diseases, they are also known causes of human cancers such as colorectal cancer. This Special Issue welcomes original research, reviews, etc., at the molecular level, genome-wide scale, or in silico study contributions to report advances in the field. The goal is to encompass the genetic and epigenetic basis of physiological and disease activity of all elements of the GI tract, and to include lessons to be learned from human and animals alike. As a landmark of this multifaceted approach, this research will benefit from the lab to clinic, given that the discovery and validation of diagnostic and potentially therapeutic biomarkers for these unclear pathologies is paramount.

Dr. Kostas A. Triantaphyllopoulos
Guest Editor

Manuscript Submission Information

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Keywords

  • gene
  • epigenetic
  • biomarker
  • intestinal
  • gut
  • IBD
  • mycobacterium avium
  • Johne’s disease

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Published Papers (1 paper)

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Research

16 pages, 3143 KiB  
Article
Activation and Functions of Col6a1+ Fibroblasts in Colitis-Associated Cancer
by Niki Chalkidi, Maria-Theodora Melissari, Ana Henriques, Athanasia Stavropoulou, George Kollias and Vasiliki Koliaraki
Int. J. Mol. Sci. 2024, 25(1), 148; https://doi.org/10.3390/ijms25010148 - 21 Dec 2023
Cited by 2 | Viewed by 1661
Abstract
Cancer-associated fibroblasts (CAFs) comprise a group of heterogeneous subpopulations with distinct identities indicative of their diverse origins, activation patterns, and pro-tumorigenic functions. CAFs originate mainly from resident fibroblasts, which are activated upon different stimuli, including growth factors and inflammatory mediators, but the extent [...] Read more.
Cancer-associated fibroblasts (CAFs) comprise a group of heterogeneous subpopulations with distinct identities indicative of their diverse origins, activation patterns, and pro-tumorigenic functions. CAFs originate mainly from resident fibroblasts, which are activated upon different stimuli, including growth factors and inflammatory mediators, but the extent to which they also maintain some of their homeostatic properties, at least at the earlier stages of carcinogenesis, is not clear. In response to cytokines, such as interleukin 1 (IL-1) and tumor necrosis factor (TNF), as well as microbial products, CAFs acquire an immunoregulatory phenotype, but its specificity and pathophysiological significance in individual CAF subsets is yet to be determined. In this study, we analyzed the properties of Col6a1-positive fibroblasts in colitis-associated cancer. We found that Col6a1+ cells partly maintain their homeostatic features during adenoma development, while their activation is characterized by the acquisition of a distinct proangiogenic signature associated with their initial perivascular location. In vitro and in vivo experiments showed that Col6a1+ cells respond to innate immune stimuli and exert pro-tumorigenic functions. However, Col6a1+-specific inhibition of TNF receptor 1 (TNFR1) or IL-1 receptor (IL-1R) signaling does not significantly affect tumorigenesis, suggesting that activation of other subsets acts in a compensatory way or that multiple immune stimuli are necessary to drive the proinflammatory activation of this subset. In conclusion, our results show that adenoma-associated CAF subsets can partly maintain the properties of homeostatic fibroblasts while they become activated to support tumor growth through distinct and compensatory mechanisms. Full article
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

1. Title: The Gut Microbiome: A New Frontier in Neurological Disease Research

Author: Mohammad Sarif Mohiuddin 

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