Gut Microbiota, Macrophages and Diet: An Intriguing New Triangle in Intestinal Fibrosis.

Asma Amamou,Guillaume Savoye,Rachel Marion-Letellier,Cian O’Mahony,Mathilde Leboutte,Subrata Ghosh

doi:10.3390/microorganisms10030490

Asma Amamou, Guillaume Savoye + Show 4 more

Open Access

https://doi.org/10.3390/microorganisms10030490

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Journal: Microorganisms	Publication Date: Feb 22, 2022
Citations: 13	License type: CC BY 4.0

Affiliation: University College Cork, University of Rouen, Inserm

Abstract

Intestinal fibrosis is a common complication in inflammatory bowel disease (IBD) without specific treatment. As macrophages are the key actors in inflammatory responses and the wound healing process, they have been extensively studied in chronic diseases these past decades. By their exceptional ability to integrate diverse stimuli in their surrounding environment, macrophages display a multitude of phenotypes to underpin a broad spectrum of functions, from the initiation to the resolution of inflammation following injury. The hypothesis that distinct macrophage subtypes could be involved in fibrogenesis and wound healing is emerging and could open up new therapeutic perspectives in the treatment of intestinal fibrosis. Gut microbiota and diet are two key factors capable of modifying intestinal macrophage profiles, shaping their specific function. Defects in macrophage polarisation, inadequate dietary habits, and alteration of microbiota composition may contribute to the development of intestinal fibrosis. In this review, we describe the intriguing triangle between intestinal macrophages, diet, and gut microbiota in homeostasis and how the perturbation of this discreet balance may lead to a pro-fibrotic environment and influence fibrogenesis in the gut.

Highlights

Inflammatory bowel diseases (IBD) are chronic relapsing and remitting inflammatory diseases affecting the gastrointestinal tract, resulting from complex interactions between genes, environment exposure, especially food, the immune system, and gut microbiota.IBD are often progressive and lifelong pathologies leading to irreversible intestinal damage causing disability and morbidity in patients [1]
During the last phase of wound healing, IL-10 is a key anti-inflammatory cytokine produced during the proliferative stage of repair that facilitates tissue remodelling by activating M2b macrophages which release metalloprotease matrix proteins (MMPs) to regulate extracellular matrix (ECM) degradation
These results suggested that dietary salt could be contributing to intestinal fibrosis progression

Summary

Introduction

Inflammatory bowel diseases (IBD) are chronic relapsing and remitting inflammatory diseases affecting the gastrointestinal tract, resulting from complex interactions between genes, environment exposure, especially food, the immune system, and gut microbiota. IBD are often progressive and lifelong pathologies leading to irreversible intestinal damage causing disability and morbidity in patients [1]. Among these complications, intestinal fibrosis is the most common. Intestinal fibrosis is characterised by exaggerated scar tissue formation in intestinal mucosa resulting from chronic inflammation. We highlight the role of macrophages in intestinal fibrogenesis and their interactions with intestinal microbiota and. Microorganisms 2022, 10, 490 diet and discuss the potential future directions of treatments by exploiting macrophage function and plasticity

Macrophages as Key Players in Fibrogenesis

Factors That Influence Macrophage Polarisation in Inflammation and Fibrosis

Gut Microbiota

Reprogramming Macrophages for Treatment of Fibrosis

Findings

Conclusions