Making Sense of Quorum Sensing at the Intestinal Mucosal Interface

Abstract

The gut microbiome can produce metabolic products that exert diverse activities, including effects on the host. Short chain fatty acids and amino acid derivatives have been the focus of many studies, but given the high microbial density in the gastrointestinal tract, other bacterial products such as those released as part of quorum sensing are likely to play an important role for health and disease. In this review, we provide of an overview on quorum sensing (QS) in the gastrointestinal tract and summarise what is known regarding the role of QS molecules such as auto-inducing peptides (AIP) and acyl-homoserine lactones (AHL) from commensal, probiotic, and pathogenic bacteria in intestinal health and disease. QS regulates the expression of numerous genes including biofilm formation, bacteriocin and toxin secretion, and metabolism. QS has also been shown to play an important role in the bacteria–host interaction. We conclude that the mechanisms of action of QS at the intestinal neuro–immune interface need to be further investigated.

Differential Proteomic Analysis of Listeria monocytogenes during High-Pressure Processing

“…The autoinducers responsible for quorum sensing are the extracellular and small diffusible signal molecules secreted by both Gram-positive and Gram-negative bacteria. More recently, quorum sensing makes microbial density in the gastrointestinal mucosal interface and plays a key role for host health and disease [ 41 ]. These molecules are used for ‘quorum sensing’ of bacteria to synchronize biofilm formation, motility, invasion, virulence, survival, and metabolism.…”

Microbes, oxytocin and stress: Converging players regulating eating behavior

“…The gut microbiota includes trillions of microbes including bacteria, archaea, viruses, and fungi that inhabit the gastrointestinal (GI) tract 48 . Through their interactions with diet, they produce numerous soluble mediators and cell wall components that have been shown to modulate gastrointestinal physiology, immune and metabolic function, brain‐gut communication, and behavior 49–52 …”

“…These bacterial metabolites could also modulate the systemic immune system either directly or via gut‐brain mediated pathways (i.e., neuroendocrine, vagal, immune) that affect central immunity and subsequent Oxt signaling 16 . Alternatively, bacteria can modulate the secretion of neurotransmitters and peptides from hormone‐releasing cells in the intestinal epithelium (serotonin, cholecystokinin, glucagon‐like peptide, ghrelin) and the enteric nervous system that regulate gut‐brain signaling 60 as well as intestinal physiology 52,61 . This, in turn, affects the availability and absorption of nutrients, microbiota composition and thus, gut‐brain communication 62 .…”

“…48 Through their interactions with diet, they produce numerous soluble mediators and cell wall components that have been shown to modulate gastrointestinal physiology, immune and metabolic function, brain-gut communication, and behavior. [49][50][51][52] Microbiota status and probiotics have been shown to affect Oxt levels, Oxt and Oxtr expression (Table 1). For example, mice treated with antibiotics for >1 month displayed decreased Oxtr expression levels in the frontal cortex and a trend for increased Oxt expression in the hypothalamus.…”

“…16 Alternatively, bacteria can modulate the secretion of neurotransmitters and peptides from hormone-releasing cells in the intestinal epithelium (serotonin, cholecystokinin, glucagon-like peptide, ghrelin) and the enteric nervous system that regulate gut-brain signaling 60 as well as intestinal physiology. 52,61 This, in turn, affects the availability and absorption of nutrients, microbiota composition and thus, gut-brain communication. 62 In addition to affecting central oxytocinergic neurons, the microbiota may also modulate enteric neurons that express Oxt or intestinal Oxtr.…”