Abstract

Among numerous molecules found in the gut ecosystem, quorum sensing (QS) molecules represent an overlooked part that warrants highlighting. QS relies on the release of small molecules (auto-inducers) by bacteria that accumulate in the environment depending on bacterial cell density. These molecules not only are sensed by the microbial community but also interact with host cells and contribute to gut homeostasis. It therefore appears entirely appropriate to highlight the role of these molecules on the immune system in dysbiosis-associated inflammatory conditions where the bacterial populations are imbalanced. Here, we intent to focus on one of the most studied QS molecule family, namely, the type I auto-inducers represented by N-acyl-homoserine lactones (AHL). First described in pathogens such as Pseudomonas aeruginosa, these molecules have also been found in commensals and have been recently described within the complex microbial communities of the mammalian intestinal tract. In this mini-review, we will expound on this emergent field of research. We will first recall evidence on AHL structure, synthesis, receptors, and functions regarding interbacterial communication. Then, we will discuss their interactions with the host and particularly with agents of the innate and adaptive gut mucosa immunity. This will reveal how this new set of molecules, driven by microbial imbalance, can interact with inflammation pathways and could be a potential target in inflammatory bowel disease (IBD). The discovery of the general impact of these compounds on the detection of the bacterial quorum and on the dynamic and immune responses of eukaryotic cells opens up a new field of pathophysiology.

Highlights

  • Dysbiosis in inflammatory bowel disease (IBD) is characterized by a reduction in bacterial biodiversity

  • LuxI synthesizes the Acyl-homoserines lactones (AHL), the molecule freely diffuses in the environment, and LuxR detects the auto-inducer, which acts as a transcription factor [14] (Figure 1)

  • As mentioned earlier, when macrophages are in a proinflammatory context, 3-oxo-C12HSL can modulate the NF-κB pathway resulting in a decrease in the expression of proinflammatory cytokines such as tumor necrosis factor-α (TNFα), regulated upon activation, normal T cell expressed, and secreted (RANTES), or monocyte chemoattractant protein-1 (MCP-1) [48]

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Summary

Introduction

Dysbiosis in inflammatory bowel disease (IBD) is characterized by a reduction in bacterial biodiversity. Quorum Sensing and Gut Immunity bacteria–bacteria communication, QS molecules are involved in interkingdom interplay between gut bacteria and host cells. In the early 2000s, researchers investigated the impact of AHL on plant physiology [4] showing that the presence of these molecules produced by soil bacteria can induce plant benefits [5] such as induction of the immune system to resist pathogens [6, 7].

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