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Eukaryotic organisms coevolved with microbes from the environment forming holobiotic meta-genomic units. Members of host-associated microbiomes have commensalic, beneficial/symbiotic, or pathogenic phenotypes. More than 100 years ago, Lorenz Hiltner, pioneer of soil microbiology, introduced the term 'Rhizosphere' to characterize the observation that a high density of saprophytic, beneficial, and pathogenic microbes are attracted by root exudates. The balance between these types of microbes decide about the health of the host. Nowadays we know, that for the interaction of microbes with all eukaryotic hosts similar principles and processes of cooperative and competitive functions are in action. Small diffusible molecules like (phyto)hormones, volatiles and quorum sensing signals are examples for mediators of interspecies and cross-kingdom interactions. Quorum sensing of bacteria is mediated by different autoinducible metabolites in a density-dependent manner. In this perspective publication, the role of QS-related activities for the health of hosts will be discussed focussing mostly on N -acyl-homoserine lactones (AHL). It is also considered that in some cases very close phylogenetic relations exist between plant beneficial and opportunistic human pathogenic bacteria. Based on a genome and system-targeted new understanding, sociomicrobiological solutions are possible for the biocontrol of diseases and the health improvement of eukaryotic hosts. [ABSTRACT FROM AUTHOR]

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Quorum sensing (QS) is one of the most well-studied cell-to-cell communication mechanisms in microorganisms. This intercellular communication process in Saccharomyces cerevisiae began to attract more and more attention for researchers since 2006, and phenylethanol, tryptophol, and tyrosol have been proven to be the main quorum sensing molecules (QSMs) of S. cerevisiae. In this paper, the research history and hotspots of QS in S. cerevisiae are reviewed, in particular, the QS system of S. cerevisiae is introduced from the aspects of regulation mechanism of QSMs synthesis, influencing factors of QSMs production, and response mechanism of QSMs. Finally, the employment of QS in adaptation to stress, fermentation products increasing, and food preservation in S. cerevisiae was reviewed. This review will be useful for investigating the microbial interactions of S. cerevisiae, will be helpful for the fermentation process in which yeast participates, and will provide an important reference for future research on S. cerevisiae QS. [ABSTRACT FROM AUTHOR]

Quorum sensing (QS) is a communication mechanism between microorganisms originally found in bacteria. In recent years, an important QS mechanism has been discovered in the field of fungi, namely, the lipoxygenase compound oxylipin of arachidonic acid acts as a QS molecule in life cycle control, particularly in the sexual and asexual development of fungi. However, the role of oxylipins in mediating eukaryotic communication has not been previously described. In this paper, we review the regulatory role of oxylipins and the underlying mechanisms and discuss the potential for application in major fungi. The role of oxylipin as a fungal quorum‐sensing molecule is the main focus of the review. Besides, the quorum regulation of fungal morphological transformation, biofilm formation, virulence factors, secondary metabolism, infection, symbiosis, and other physiological behaviors are discussed. Moreover, future prospectives and applications are elaborated as well. [ABSTRACT FROM AUTHOR]

Inflammatory Bowel Disease (IBD) is an enduring inflammatory disease of the gastrointestinal tract (GIT). The complexity of IBD, its profound impact on patient's quality of life, and its burden on healthcare systems necessitate continuing studies to elucidate its etiology, refine care strategies, improve treatment outcomes, and identify potential targets for novel therapeutic interventions. The discovery of a connection between IBD and gut bacterial quorum sensing (QS) molecules has opened exciting opportunities for research into IBD pathophysiology. QS molecules are small chemical messengers synthesized and released by bacteria based on population density. These chemicals are sensed not only by the microbial species but also by host cells and are essential in gut homeostasis. QS molecules are now known to interact with inflammatory pathways, therefore rendering them potential therapeutic targets for IBD management. Given these intriguing developments, the most recent research findings in this area are herein reviewed. First, the global burden of IBD and the disruptions of the gut microbiota and intestinal barrier associated with the disease are assessed. Next, the general QS mechanism and signaling molecules in the gut are discussed. Then, the roles of QS molecules and their connection with IBD are elucidated. Lastly, the review proposes potential QS-based therapeutic targets for IBD, offering insights into the future research trajectory in this field. [Display omitted] • The connection between IBD and gut bacterial QS molecules opens exciting opportunities for IBD pathophysiology research. • QS molecules interact with inflammatory pathways, rendering them potential therapeutic targets for IBD management. • 3-oxo-C12:2-HSL exerts anti-inflammatory and tight junction integrity-preserving characteristics. • Aryl hydrocarbon receptors (AhR) and paraoxonases (PONs) are observed to be dysfunctional in several IBD patients. • 3-oxo-C12:2-HSL molecule, AhR, and PONs may be explored as promising targets for IBD management. [ABSTRACT FROM AUTHOR]

In this study, we investigated the activation of TRPV1 and TRPA1 by N -acyl homoserine lactones, quorum sensing molecules produced by Gram-negative bacteria, and the inhibitory effect of TRPV1 and TRPA1 by autoinducing peptides (AIPs), quorum sensing molecules produced by Gram-positive bacteria, using human embryonic kidney 293T cell lines stably expressing human TRPV1 and TRPA1, respectively. As a result, we found that some N -acyl homoserine lactones, such as N -octanoyl-L-homoserine lactone (C8-HSL), N -nonanoyl-L-homoserine lactone (C9-HSL) and N -decanoyl-L-homoserine lactone (C10-HSL), activated both TRPV1 and TRPA1. In addition, we clarified that some N -acyl homoserine lactones, such as N -3-oxo-dodecanoyl-L-homoserine lactone (3-oxo-C12-HSL), only activated TRPV1 and N -acyl homoserine lactones having saturated short acyl chain, such as N -acetyl-L-homoserine lactone (C2-HSL) and N -butyryl-L-homoserine lactone (C4-HSL), only activated TRPA1. Furthermore, we found that an AIP, simple linear peptide CHWPR, inhibited both TRPV1 and TRPA1 and peptide having thiolactone ring DICNAYF, the thiolactone ring were formed between C3 to F7, strongly inhibited only the TRPV1. Although the specificity of TRPV1 and TRPA1 for quorum sensing molecules was different, these data suggest that both TRPV1 and TRPA1 would function as receptors for quorum sensing molecule produced by bacteria. Graphical Abstract [ABSTRACT FROM AUTHOR]

Orthopedic implant-related bacterial infections and resultant antibiotic-resistant biofilms hinder implant-tissue integration and failure. Biofilm quorum sensing (QS) communication determines the pathogen colonization success. However, it remains unclear how implant modifications and host cells are influenced by, or influence, QS. High aspect ratio nanotopographies have shown to reduce biofilm formation of Pseudomonas aeruginosa , a sepsis causing pathogen with well-defined QS molecules. Producing such nanotopographies in relevant orthopedic materials (i.e., titanium) allows for probing QS using mass spectrometry-based metabolomics. However, nanotopographies can reduce host cell adhesion and regeneration. Therefore, we developed a polymer (poly(ethyl acrylate), PEA) coating that organizes extracellular matrix proteins, promoting bioactivity to host cells such as human mesenchymal stromal cells (hMSCs), maintaining biofilm reduction. This allowed us to investigate how hMSCs, after winning the race for the surface against pathogenic cells, interact with the biofilm. Our approach revealed that nanotopographies reduced major virulence pathways, such as LasR. The enhanced hMSCs support provided by the coated nanotopographies was shown to suppress virulence pathways and biofilm formation. Finally, we selected bioactive metabolites and demonstrated that these could be used as adjuncts to the nanostructured surfaces to reduce biofilm formation and enhance hMSC activity. These surfaces make excellent models to study hMSC-pathogen interactions and could be envisaged for use in novel orthopedic implants.

Quorum sensing (QS) is the ability of some bacteria to detect and to respond to population density through signalling molecules. QS molecules are involved in motility and cell aggregation mechanisms in diseases such as sepsis. Few biomarkers are currently available to diagnose sepsis, especially in high-risk conditions. The aim of this study was the development of new analytical methods based on liquid chromatography-mass spectrometry for the detection and quantification of QS signalling molecules, including N-acyl homoserine lactones (AHL) and hydroxyquinolones (HQ), in biofluids. Biological samples used in the study were Pseudomonas aeruginosa bacterial cultures and plasma from patients with sepsis. We developed two MS analytical methods, based on neutral loss (NL) and product ion (PI) experiments, to identify and characterize unknown AHL and HQ molecules. We then established a multiple-reaction-monitoring (MRM) method to quantify specific QS compounds. We validated the HPLC-MS-based approaches (MRM-NL-PI), and data were in accord with the validation guidelines. With the NL and PI MS-based methods, we identified and characterized 3 and 13 unknown AHL and HQ compounds, respectively, in biological samples. One of the newly found AHL molecules was C12-AHL, first quantified in Pseudomonas aeruginosa bacterial cultures. The MRM quantitation of analytes in plasma from patients with sepsis confirmed the analytical ability of MRM for the quantification of virulence factors during sepsis. [ABSTRACT FROM AUTHOR]

Aspergillus fumigatus is an opportunistic fungal pathogen to which immunocompromised patients are especially susceptible. A. fumigatus can form biofilms both in vitro and in vivo. Quorum sensing molecules (QSMs) have activity against some fungi. This study aimed to determine the activity of the QSMs farnesol, tyrosol, phenylethanol and tryptophol against the growth A. fumigatus on solid media, and against its ability to form biofilms. The activity of each QSM against planktonic A. fumigatus growth was assessed using the CLSI M38-A2 broth microdilution assay, while QSM inhibition of A. fumigatus's biofilm formation was measured in crystal violet, and 2, 3-bis (2-methoxy-4-nitro-5-sulfo-phenyl)-2Htetrazolium-5-caboxanilide (XTT) assays. The QSMs reduced the colony diameter of the studied strains in a QSM-dependent pattern. Tryptophol showed the best effect and tyrosol showed the poorest effect. The minimum inhibitory concentrations (MICs) for farnesol, tyrosol, phenylethanol and tryptophol tested against A. fumigatus were > 32, > 32, 16 and 8 mM, respectively. The effective concentration each QSM required to inhibit A. fumigatus biofilm formation were higher than the planktonic MICs. In this study, the performance of QSMs against A. fumigatus ranked from best to worst as follows: tryptophol, phenylethanol, farnesol and tyrosol. Because of phenylethanol and tryptophol showed the strongest effect to the growth and biofilm formation of A. fumigatus. Therefore, the cytotoxic activities of phenylethanol and tryptophol in A549 cells (lung alveolar epithelial cells) were determined. However, phenylethanol and tryptophol induced A549 cell damage (at MIC level), as demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium (MTT) and lactate dehydrogenase (LDH) assays. [ABSTRACT FROM AUTHOR]

The gut microbiota exerts a mutualistic interaction with the host in a fragile ecosystem and the host intestinal, neural, and immune cells. Perturbations of the gastrointestinal track composition after stress have profound consequences on the central nervous system and the immune system. Reciprocally, brain signals after stress affect the gut microbiota highlighting the bidirectional communication between the brain and the gut. Here, we focus on the potential role of inflammation in mediating stress-induced gut-brain changes and discuss the impact of several immune cells and inflammatory molecules of the gut-brain dialogue after stress. Understanding the impact of microbial changes on the immune system after stress might provide new avenues for therapy.

Although there has been a significant amount of research focused on the pathophysiology of spinal cord injury (SCI), there is limited information on the consequences of SCI on remote organs. SCI can produce significant effects on a variety of organ systems, including the gastrointestinal tract. Patients with SCI often suffer from severe, debilitating bowel dysfunction in addition to their physical disabilities, which is of major concern for these individuals because of the adverse impact on their quality of life. Herein, we report on our investigation into the effects of SCI and subsequent antibiotic treatment on the intestinal tissue and microbiota. For that, we used a thoracic SCI rat model and investigated changes to the microbiota, proinflammatory cytokine levels, and bacterial communication molecule levels post-injury and gentamicin treatment for 7 days. We discovered significant changes, the most interesting being the differences in the gut microbiota beta diversity of 8-week SCI animals compared to control animals at the family, genus, and species level. Specifically, 35 operational taxonomic units were enriched in the SCI animal group and three were identified at species level; Lactobacillus intestinalis, Clostridium disporicum, and Bifidobacterium choerinum. In contrast, Clostridium saccharogumia was identified as depleted in the SCI animal group. Proinflammatory cytokines interleukin (IL)-12, macrophage inflammatory protein-2 (MIP-2), and tumor necrosis factor alpha were found to be significantly elevated in intestinal tissue homogenate 4 weeks post-SCI compared to 8-weeks post-injury. Further, levels of IL-1β, IL-12, and MIP-2 significantly correlated with changes in beta diversity 8-weeks post-SCI. Our data provide a greater understanding of the early effects of SCI on the microbiota and gastrointestinal tract, highlighting the need for further investigation to elucidate the mechanism underlying these effects. [ABSTRACT FROM AUTHOR]

Cultivating microalgae using wastewater is an economical strategy to produce biofuel; however, microbial contamination has to be controlled strictly. Microalgae lipid accumulation can be triggered by environmental pressures, and here, we studied whether microbial contamination is the pressure for microalgae. We hypothesized this pressure was forced via cell-to-cell communication with quorum sensing molecules (QSMs). In this work, we verified the impacts of QSMs produced by activated sludge (wastewater-born microbial consortiums) on both lipid content and biomass production of the microalgae Chlorophyta sp., since in combination, they determined lipid productivity. With QSMs stress, the lipid content of Chlorophyta sp. increased by ∼84%, while biomass production decreased only slightly. Consistently, enzymes on the fatty acid synthesis pathways were generally up-regulated, while they were slightly down-regulated for DNA replication. In summary, the total lipid production improved by 86%. These results revealed the positive effects of microbial contamination on microalgae biofuel production. [ABSTRACT FROM AUTHOR]

[Display omitted] Many human fungal pathogens are opportunistic. They are primarily benign residents of the human body and only become infectious when the host's immunity and microbiome are compromised. Bacteria dominate the human microbiome, playing an essential role in keeping fungi harmless and acting as the first line of defense against fungal infection. The Human Microbiome Project, launched by NIH in 2007, has stimulated extensive investigation and significantly advanced our understanding of the molecular mechanisms governing the interaction between bacteria and fungi, providing valuable insights for developing future antifungal strategies by exploiting the interaction. This review summarizes recent progress in this field and discusses new possibilities and challenges. We must seize the opportunities presented by researching bacterial-fungal interplay in the human microbiome to address the global spread of drug-resistant fungal pathogens and the drying pipelines of effective antifungal drugs. [ABSTRACT FROM AUTHOR]

The halogenation of quorum sensing molecules (QSMs) is known to be catalyzed by enzymes such as haloperoxidase (HPO) as well as cerium dioxide nanocrystals (NC), which mimic enzymes. Those enzymes and mimics can influence biological processes such as biofilm formation, where bacteria use QSMs for the "chemical" communication between each other and the coordination of surface colonization. However, not much is known about the degradation behavior of a broad spectrum of QSMs, especially for HPO and its mimics. Therefore, in this study, the degradation of three QSMs with different molecule moieties was elucidated. For this purpose, different batch experiments were carried out with HPOs, NCs and free active bromine (FAB). For N -β-ketocaproyl-homoserine lactone (3-Oxo-C 6 -AHL), N - cis -tetradec-9 Z -enoyl-homoserine lactone (C 14:1 -AHL) and 2-heptyl-4-quinolone (HHQ) a fast degradation and moiety-specific transformations were observed. The HPO vanadium bromoperoxidase as well as cerium dioxide NCs catalyzed the formation of the same brominated transformation products (TPs). Since the same TPs are formed in batch experiments with FAB it is very likely that FAB is playing a major role in the catalytical reaction mechanism leading to the transformation of QSMs. In this study in total 17 TPs could be identified in different levels of confidence and the catalytic degradation processes for two QS groups (unsaturated AHLs and alkyl quinolones) with cerium dioxide NCs and vanadium bromoperoxidase were expanded.

The interplay of sourdough microbiology and generated volatile compounds that define its sensory characteristics was studied. In order to detail the flavour generating potential of microorganisms, eight single-strain dough fermentations were studied, four of them never investigated before. Moreover, for the first time, both ex-novo and traditional wheat sourdoughs were investigated and compared to chemically acidified dough. HS-SPME-GC-MS was used to sample and analyse volatile compounds, some of which have never been detected before in sourdoughs. Alcohols, esters, carbonyl compounds, and acids mainly characterised the volatile profiles. Different sourdough microbiota resulted in different volatile profiles. PCA indicated that samples could be clustered according to their specific microbiota. Production of aroma compounds was strain-specific, confirming previous findings. This study can contribute to the management of desirable features and differentiate specialty products, as well as selecting new, suitable, sourdoughs after microbial screening. [ABSTRACT FROM AUTHOR]

This investigation documents the expression of the in vivo dimorphic program exhibited by the insect mycopathogen Metarhizium rileyi . This insect mycopathogen represents the key mortality factor regulating various caterpillar populations in legumes, including subtropical and tropical soybeans. Using two hosts and M. rileyi isolates, we have measured M. rileyi growth rates under in vivo and in vitro conditions and have assessed the pathogen’s impact on host fitness. Significantly, the hyphal bodies-to-mycelia transition that occurs at the late infection stage is regulated by a quorum-sensing molecule(s) (QSM) that triggers hyphal bodies (Hb) to synchronously switch to the tissue-invasive mycelia. Within hours of this transition, the host insect succumbs to mycosis. The production of the QS chemical(s) occurs when a quorum of Hb is produced in the hemolymph (late-stage infection). Furthermore, the QS activity detected in late-stage infected sera is unique and is unrelated to any known fungal QSM. The lack of similar QS activity from conditioned media of M. rileyi suggests that the chemical signal(s) that mediates the dimorphic switch is produced by host tissues in response to a quorum of hyphal bodies produced in the host hemolymph. The serum-based QS activity is retained after lyophilization, mild heat treatment, and proteinase digestion. However, attempts to extract/identify the QSM have been unsuccessful. Results suggest that the observed hyphal body-to-mycelia transition is a multi-step process involving more than one chemical signal. [ABSTRACT FROM AUTHOR]

Quorum sensing (QS) activity in Ophiostoma fungi has not been described. We have examined the growth conditions on the control of dimorphism in Ophiostoma floccosum, an attractive biocontrol agent against blue-stain fungi, and its relationship with QS activity. In a defined culture medium with l-proline as the N source, a high inoculum size (10 c.f.u. ml) was the principal factor that promoted yeast-like growth. Inoculum size effect can be explained by the secretion of a QS molecule(s) (QSMs) responsible for inducing yeast morphology. QSM candidates were extracted from spent medium and their structure was determined by GC-MS. Three cyclic sesquiterpenes were found. The most abundant molecule, and therefore the principal candidate to be the QSM responsible for yeast growth of O. floccosum, was 1,1,4a-trimethyl-5,6-dimethylene-decalin (CH). Other two compounds were also detected. [ABSTRACT FROM AUTHOR]

Abstract: When bacteria colonize surfaces, they socialize and form biofilms. This process is well regulated and relies on the communication among the bacteria via so-called “quorum sensing molecules”. Among those, N-(3-oxododecanoyl)-l-homoserine lactone (AHL-12), generated by Pseudomonas aeruginosa and other Gram-negative bacteria, activates not only bacteria but also interacts with mammalian cells. Among others, it activates phagocytic cells and – as we had shown previously – it is chemotactic for human polymorphonuclear neutrophils (PMN) in vitro. In the present study, we analyzed the signalling pathway of AHL-12 in PMN. We focused on the mitogen activated protein (MAP) kinase p38, because SB203580, an inhibitor of p38, prevented the AHL-12 induced chemotaxis. We found that in response to AHL-12, p38 was phosphorylated within minutes, as was its downstream target, the MAPKAP-Kinase-2 (MK2). In PMN, the major substrate of MK2 is the leukocyte specific protein 1 (LSP1), which binds to F-actin and participates directly in actin polymerization and cell migration. In response to AHL-12, LSP1 was phosphorylated and co-localized with F-actin in polarized PMN, suggesting that AHL-12-induced migration depended on p38 and LSP1 activation. [Copyright &y& Elsevier]

Over the past two decades there have been great advances in biotechnology, including use of nucleic acids, proteins, and whole cells to develop a variety of molecular analytical tools for diagnostic, screening, and pharmaceutical applications. Through manipulation of bacterial plasmids and genomes, bacterial whole-cell sensing systems have been engineered that can serve as novel methods for analyte detection and characterization, and as more efficient and cost-effective alternatives to traditional analytical techniques. Bacterial cell-based sensing systems are typically sensitive, specific and selective, rapid, easy to use, low-cost, and amenable to multiplexing, high-throughput, and miniaturization for incorporation into portable devices. This critical review is intended to provide an overview of available bacterial whole-cell sensing systems for assessment of a variety of clinically relevant analytes. Specifically, we examine whole-cell sensing systems for detection of bacterial quorum sensing molecules, organic and inorganic toxic compounds, and drugs, and for screening of antibacterial compounds for identification of their mechanisms of action. Methods used in the design and development of whole-cell sensing systems are also reviewed. [ABSTRACT FROM AUTHOR]

Introduction. Pseudomonas aeruginosa produces quorum sensing signalling molecules including 2-alkyl-4-quinolones (AQs), which regulate virulence factor production in the cystic fibrosis (CF) airways. Hypothesis/Gap statement. Culture can lead to condition-dependent artefacts which may limit the potential insights and applications of AQs as minimally-invasive biomarkers of bacterial load. Aim. We aimed to use culture-independent methods to explore the correlations between AQ levels and live P. aeruginosa load in adults with CF. Methodology. Seventy-five sputum samples at clinical stability and 48 paired sputum samples obtained at the beginning and end of IV antibiotics for a pulmonary exacerbation in adults with CF were processed using a viable cell separation technique followed by quantitative P. aeruginosa polymerase chain reaction (qPCR). Live P. aeruginosa qPCR load was compared with the concentrations of three AQs (HHQ, NHQ and HQNO) detected in sputum, plasma and urine. Results. At clinical stability and the beginning of IV antibiotics for pulmonary exacerbation, HHQ, NHQ and HQNO measured in sputum, plasma and urine were consistently positively correlated with live P. aeruginosa qPCR load in sputum, compared to culture. Following systemic antibiotics live P. aeruginosa qPCR load decreased significantly ( P <0.001) and was correlated with a reduction in plasma NHQ (plasma: r=0.463, P =0.003). Conclusion. In adults with CF, AQ concentrations correlated more strongly with live P. aeruginosa bacterial load measured by qPCR compared to traditional culture. Prospective studies are required to assess the potential of systemic AQs as biomarkers of P. aeruginosa bacterial burden.

Skeletal muscle makes up the largest part of human body mass and a good maintenance of this organ is essential for general health. In accordance, muscle wasting, a frequent phenomenon in many diseases, is associated with functional decline and a decrease in quality of life. Unfortunately, due to a lack of knowledge of the underlying pathophysiology, no targeted therapies exist today to encounter muscle wasting. Recent studies suggest a role for the gut microbiome in muscle wasting, without the mediators of this gut-muscle axis being identified. Here we evaluated the possible effects of 75 quorum sensing molecules (QSM), traditionally only seen as intra-bacterial communication molecules, on C2C12 muscle cells, studying viability, differentiation, inflammation, mitochondrial changes and protein degradation as biological outcomes. The responses were evaluated using different approaches: median absolute deviation, quartiles, strictly standardized mean difference and robust strictly standardized mean difference. This study resulted in 30 QSM, with effects observed on C2C12 cells. Known producers of the 27 peptide QSM belong to species of the genus Staphylococcus , Streptococcus , Enterococcus , Bacillus , Lactobacillus and Escherichia , while the 3 non-peptide QSM are produced by a broad range of Gram-positive and Gram-negative bacteria. Altogether, these proof-of-concept findings provide the first evidence that QSM produced by microbiota play a role in the gut-muscle axis, opening new perspectives for diagnostic and therapeutic targets in muscle wasting diseases. • Quorum Sensing Molecules (QSM) effect C2C12 muscle cells. • Effects are mostly on muscle viability and inflammation. • A proof-of-concept that QSM are part of the gut-muscle axis [ABSTRACT FROM AUTHOR]

Quorum-sensing molecules (QSMs) are secreted by bacteria to signal population density. Upon reaching a critical concentration, QSMs induce transcriptional alterations in bacteria, which enable virulence factor expression and biofilm formation. It is unclear whether mammalian hosts can recognize QSMs to trigger responsive antibacterial immunity. We report that mouse mast-cell-specific G-protein-coupled receptor Mrgprb2 and its human homolog MRGPRX2 are receptors for Gram-positive QSMs, including competence-stimulating peptide (CSP)-1. CSP-1 activates Mrgprb2 and MRGPRX2, triggering mast cell degranulation, which inhibits bacterial growth and prevents biofilm formation. Such antibacterial functions are reduced in Mrgprb2-deficient mast cells, while wild-type mast cells fail to inhibit the growth of bacterial strains lacking CSP-1. Mrgprb2 -knockout mice exhibit reduced bacterial clearance, while pharmacologically activating Mrgprb2 in vivo eliminates bacteria and improves disease score. These findings identify a host defense mechanism that uses QSMs as an "Achilles heel" and suggest MRGPRX2 as a potential therapeutic target for controlling bacterial infections. • The mammalian receptor Mrgprb2 and MRGPRX2 can detect bacterial QSMs • QSM detection by Mrgprb2 and MRGPRX2 in mast cells elicits antibacterial mediator release • Mrgprb2 recognition of QSMs is critical for an effective immune response to bacteria • Pharmacologic activation of Mrgprb2 and MRGPRX2 enhances bacterial clearance Bacteria use quorum-sensing signaling for cross-species communication. Pundir et al. report that host mast cells detect Gram-positive-bacteria-derived quorum-sensing molecules via the Mrgpr receptors. Mrgpr activation triggers antibacterial activity and immune cell recruitment to efficiently clear bacteria, while animals deficient in Mrgpr are hypersusceptible to bacterial infection. [ABSTRACT FROM AUTHOR]