Histamine: A Bacterial Signal Molecule

Abstract

Bacteria have evolved sophisticated signaling mechanisms to coordinate interactions with organisms of other domains, such as plants, animals and human hosts. Several important signal molecules have been identified that are synthesized by members of different domains and that play important roles in inter-domain communication. In this article, we review recent data supporting that histamine is a signal molecule that may play an important role in inter-domain and inter-species communication. Histamine is a key signal molecule in humans, with multiple functions, such as being a neurotransmitter or modulator of immune responses. More recent studies have shown that bacteria have evolved different mechanisms to sense histamine or histamine metabolites. Histamine sensing in the human pathogen Pseudomonas aeruginosa was found to trigger chemoattraction to histamine and to regulate the expression of many virulence-related genes. Further studies have shown that many bacteria are able to synthesize and secrete histamine. The release of histamine by bacteria in the human gut was found to modulate the host immune responses and, at higher doses, to result in host pathologies. The elucidation of the role of histamine as an inter-domain signaling molecule is an emerging field of research and future investigation is required to assess its potential general nature.

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“…Innate and adaptive immune cells throughout the body can produce histamine by decarboxylation of the amino acid L-histidine by the enzyme histidine decarboxylase (HDC) ( Jutel et al, 2009 ). Many bacteria are able to synthesize and secrete histamine as well and histamine has been considered as another central signal molecule that mediates bacteria–host interactions ( Krell et al, 2021 ). For example, the administration of the histamine-secreting Lactobacillus rhamnosus had an anti-inflammatory effect by reducing the secretion of various interleukines and tumor necrosis factor α ( Frei et al, 2013 ).…”

Revisiting the virulence hallmarks of Pseudomonas aeruginosa: a chronicle through the perspective of quorum sensing

“…aeruginosa are intimately linked with its virulence. A classic example is histamine, a pharmacologically active compound that functions as a neurotransmitter and modulator of inflammatory reactions, allergies and autoimmune diseases (Krell et al ., 2021). Infection by P .…”

“…The pathogen performs high‐affinity chemotaxis to histamine gradients via the TlpQ, PctA and PctC chemoreceptors, thereby enabling the recruitment of bacterial cells at the infection site and driving the expression (↑) of QS‐dependent virulence genes (Corral‐Lugo et al ., 2018). These include a repertoire of genes associated with bacterial secretion systems, PQS and pyocyanin production, biofilm formation, siderophore production, secretion and iron uptake (Krell et al ., 2021). Recently, histamine has been shown to activate HinK, a LysR‐type transcriptional regulator that directly activates the genes associated with histamine uptake and metabolism, PQS biosynthesis and iron acquisition (Wang et al ., 2021).…”

“…Interestingly, the chemotactic abilities of P. aeruginosa are intimately linked with its virulence. A classic example is histamine, a pharmacologically active compound that functions as a neurotransmitter and modulator of inflammatory reactions, allergies and autoimmune diseases (Krell et al, 2021). Infection by P. aeruginosa has been shown to induce neutrophil histamine content and stimulate its secretion in murine models (Xu et al, 2012).…”

“…Infection by P. aeruginosa has been shown to induce neutrophil histamine content and stimulate its secretion in murine models (Xu et al, 2012). Histamine is not only a key modulator of the host immune system but also triggers chemoattraction and regulates virulence-related genes in P. aeruginosa (Krell et al, 2021). The pathogen performs high-affinity chemotaxis to histamine gradients via the TlpQ, PctA and PctC chemoreceptors, thereby enabling the recruitment of bacterial cells at the infection site and driving the expression (") of QS-dependent virulence genes (Corral-Lugo et al, 2018).…”