The role of gut microbiota, immune system, and autophagy in the pathogenesis of inflammatory bowel disease: Molecular mechanisms and therapeutic approaches

The crosstalk between gut microbiota, intestinal epithelial cells, and innate and adaptive immune system governs the maintenance of the intestinal homeostasis. Any interference in this tight dialogue and in the processes preserving cellular homeostasis (e.g., autophagy) may dysregulate the immune response and impair the clearance of harmful bacteria favoring the dysbiotic alteration of the microbial flora that leads to chronic inflammation. Gut dysbiosis is strongly associated with gastrointestinal inflammatory disorders, among them the inflammatory bowel disease (IBD). This review discusses the current knowledge on IBD, from the genetic background of high-risk patients to the molecular mechanisms underlying the disease, the contribution of the microbial flora, and the role of autophagy in intestinal epithelia homeostasis. Further, we illustrate the state of art regarding the targeted-nutritional approaches aimed to restore the beneficial crosstalk between an “anti-inflammatory” microbiota and the host. Analysis of the molecular pathogenesis of IBD will help identify genetic and diet-associated risk factors and thus suggest personalized strategies to prevent and manage the disease to improve quality of life with long-term maintenance of the remission phase. Schematic representation of the study. Inflammatory bowel disease (IBD) resolution through the beneficial effect of microbiota-induced autophagy on inflammation.

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Publication Details

Journal
Aspects of Molecular Medicine
Published
2024-10-17
DOI
https://doi.org/10.1016/j.amolm.2024.100056
Citations
27
Primary Topic
Gut microbiota and health
Type
article
Field-Weighted Citation Impact
6.31
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article

The role of gut microbiota, immune system, and autophagy in the pathogenesis of inflammatory bowel disease: Molecular mechanisms and therapeutic approaches

Beatrice Garavaglia, Ciro Isidoro, Marco Pane, Angela Amoruso et al.
27 citations
Aspects of Molecular Medicine
Gut microbiota and health
6.31
article

The role of gut microbiota, immune system, and autophagy in the pathogenesis of inflammatory bowel disease: Molecular mechanisms and therapeutic approaches

Beatrice Garavaglia, Ciro Isidoro, Marco Pane, Angela Amoruso, Alessandra Ferraresi, Letizia Vallino
article en
27 citations

Abstract

The crosstalk between gut microbiota, intestinal epithelial cells, and innate and adaptive immune system governs the maintenance of the intestinal homeostasis. Any interference in this tight dialogue and in the processes preserving cellular homeostasis (e.g., autophagy) may dysregulate the immune response and impair the clearance of harmful bacteria favoring the dysbiotic alteration of the microbial flora that leads to chronic inflammation. Gut dysbiosis is strongly associated with gastrointestinal inflammatory disorders, among them the inflammatory bowel disease (IBD). This review discusses the current knowledge on IBD, from the genetic background of high-risk patients to the molecular mechanisms underlying the disease, the contribution of the microbial flora, and the role of autophagy in intestinal epithelia homeostasis. Further, we illustrate the state of art regarding the targeted-nutritional approaches aimed to restore the beneficial crosstalk between an “anti-inflammatory” microbiota and the host. Analysis of the molecular pathogenesis of IBD will help identify genetic and diet-associated risk factors and thus suggest personalized strategies to prevent and manage the disease to improve quality of life with long-term maintenance of the remission phase. Schematic representation of the study. Inflammatory bowel disease (IBD) resolution through the beneficial effect of microbiota-induced autophagy on inflammation.

Aspects of Molecular MedicineVol. 4
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” (IT), Probiotical (Italy) (IT)
Good health and well-being
Openalex Percentile: Top 3%
Gut microbiota and health
6.31
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