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1.
Cell ; 185(22): 4170-4189.e20, 2022 10 27.
Artigo em Inglês | MEDLINE | ID: mdl-36240781

RESUMO

Nociceptive pain is a hallmark of many chronic inflammatory conditions including inflammatory bowel diseases (IBDs); however, whether pain-sensing neurons influence intestinal inflammation remains poorly defined. Employing chemogenetic silencing, adenoviral-mediated colon-specific silencing, and pharmacological ablation of TRPV1+ nociceptors, we observed more severe inflammation and defective tissue-protective reparative processes in a murine model of intestinal damage and inflammation. Disrupted nociception led to significant alterations in the intestinal microbiota and a transmissible dysbiosis, while mono-colonization of germ-free mice with Gram+Clostridium spp. promoted intestinal tissue protection through a nociceptor-dependent pathway. Mechanistically, disruption of nociception resulted in decreased levels of substance P, and therapeutic delivery of substance P promoted tissue-protective effects exerted by TRPV1+ nociceptors in a microbiota-dependent manner. Finally, dysregulated nociceptor gene expression was observed in intestinal biopsies from IBD patients. Collectively, these findings indicate an evolutionarily conserved functional link between nociception, the intestinal microbiota, and the restoration of intestinal homeostasis.


Assuntos
Microbioma Gastrointestinal , Doenças Inflamatórias Intestinais , Camundongos , Animais , Microbioma Gastrointestinal/fisiologia , Nociceptores/fisiologia , Substância P , Disbiose , Inflamação
2.
Nature ; 611(7936): 578-584, 2022 11.
Artigo em Inglês | MEDLINE | ID: mdl-36323778

RESUMO

Dietary fibres can exert beneficial anti-inflammatory effects through microbially fermented short-chain fatty acid metabolites<sup>1,2</sup>, although the immunoregulatory roles of most fibre diets and their microbiota-derived metabolites remain poorly defined. Here, using microbial sequencing and untargeted metabolomics, we show that a diet of inulin fibre alters the composition of the mouse microbiota and the levels of microbiota-derived metabolites, notably bile acids. This metabolomic shift is associated with type 2 inflammation in the intestine and lungs, characterized by IL-33 production, activation of group 2 innate lymphoid cells and eosinophilia. Delivery of cholic acid mimics inulin-induced type 2 inflammation, whereas deletion of the bile acid receptor farnesoid X receptor diminishes the effects of inulin. The effects of inulin are microbiota dependent and were reproduced in mice colonized with human-derived microbiota. Furthermore, genetic deletion of a bile-acid-metabolizing enzyme in one bacterial species abolishes the ability of inulin to trigger type 2 inflammation. Finally, we demonstrate that inulin enhances allergen- and helminth-induced type 2 inflammation. Taken together, these data reveal that dietary inulin fibre triggers microbiota-derived cholic acid and type 2 inflammation at barrier surfaces with implications for understanding the pathophysiology of allergic inflammation, tissue protection and host defence.


Assuntos
Ácidos e Sais Biliares , Fibras na Dieta , Microbioma Gastrointestinal , Inflamação , Inulina , Animais , Humanos , Camundongos , Ácidos e Sais Biliares/metabolismo , Ácido Cólico/farmacologia , Fibras na Dieta/farmacologia , Microbioma Gastrointestinal/efeitos dos fármacos , Microbioma Gastrointestinal/fisiologia , Imunidade Inata , Inflamação/induzido quimicamente , Inflamação/classificação , Inflamação/patologia , Inulina/farmacologia , Linfócitos/citologia , Linfócitos/efeitos dos fármacos , Linfócitos/imunologia , Metabolômica , Pulmão/efeitos dos fármacos , Pulmão/patologia , Intestinos/efeitos dos fármacos , Intestinos/microbiologia , Intestinos/patologia , Interleucina-33/metabolismo , Eosinófilos/citologia , Eosinófilos/efeitos dos fármacos , Eosinófilos/imunologia
3.
Nature ; 611(7937): 787-793, 2022 11.
Artigo em Inglês | MEDLINE | ID: mdl-36323781

RESUMO

Emerging studies indicate that cooperation between neurons and immune cells regulates antimicrobial immunity, inflammation and tissue homeostasis. For example, a neuronal rheostat provides excitatory or inhibitory signals that control the functions of tissue-resident group 2 innate lymphoid cells (ILC2s) at mucosal barrier surfaces1-4. ILC2s express NMUR1, a receptor for neuromedin U (NMU), which is a prominent cholinergic neuropeptide that promotes ILC2 responses5-7. However, many functions of ILC2s are shared with adaptive lymphocytes, including the production of type 2 cytokines8,9 and the release of tissue-protective amphiregulin (AREG)10-12. Consequently, there is controversy regarding whether innate lymphoid cells and adaptive lymphocytes perform redundant or non-redundant functions13-15. Here we generate a new genetic tool to target ILC2s for depletion or gene deletion in the presence of an intact adaptive immune system. Transgenic expression of iCre recombinase under the control of the mouse Nmur1 promoter enabled ILC2-specific deletion of AREG. This revealed that ILC2-derived AREG promotes non-redundant functions in the context of antiparasite immunity and tissue protection following intestinal damage and inflammation. Notably, NMU expression levels increased in inflamed intestinal tissues from both mice and humans, and NMU induced AREG production in mouse and human ILC2s. These results indicate that neuropeptide-mediated regulation of non-redundant functions of ILC2s is an evolutionarily conserved mechanism that integrates immunity and tissue protection.


Assuntos
Imunidade Inata , Mucosa Intestinal , Linfócitos , Neuropeptídeos , Animais , Humanos , Camundongos , Citocinas/imunologia , Citocinas/metabolismo , Imunidade Inata/imunologia , Inflamação/imunologia , Inflamação/parasitologia , Inflamação/patologia , Linfócitos/imunologia , Neuropeptídeos/metabolismo , Neuropeptídeos/fisiologia , Anfirregulina , Mucosa Intestinal/imunologia , Mucosa Intestinal/parasitologia , Mucosa Intestinal/patologia
4.
Nature ; 611(7937): 794-800, 2022 11.
Artigo em Inglês | MEDLINE | ID: mdl-36323785

RESUMO

Protective immunity relies on the interplay of innate and adaptive immune cells with complementary and redundant functions. Innate lymphoid cells (ILCs) have recently emerged as tissue-resident, innate mirror images of the T cell system, with which they share lineage-specifying transcription factors and effector machinery1. Located at barrier surfaces, ILCs are among the first responders against invading pathogens and thus could potentially determine the outcome of the immune response2. However, so far it has not been possible to dissect the unique contributions of ILCs to protective immunity owing to limitations in specific targeting of ILC subsets. Thus, all of the available data have been generated either in mice lacking the adaptive immune system or with tools that also affect other immune cell subsets. In addition, it has been proposed that ILCs might be dispensable for a proper immune response because other immune cells could compensate for their absence3-7. Here we report the generation of a mouse model based on the neuromedin U receptor 1 (Nmur1) promoter as a driver for simultaneous expression of Cre recombinase and green fluorescent protein, which enables gene targeting in group 2 ILCs (ILC2s) without affecting other innate and adaptive immune cells. Using Cre-mediated gene deletion of Id2 and Gata3 in Nmur1-expressing cells, we generated mice with a selective and specific deficiency in ILC2s. ILC2-deficient mice have decreased eosinophil counts at steady state and are unable to recruit eosinophils to the airways in models of allergic asthma. Further, ILC2-deficient mice do not mount an appropriate immune and epithelial type 2 response, resulting in a profound defect in worm expulsion and a non-protective type 3 immune response. In total, our data establish non-redundant functions for ILC2s in the presence of adaptive immune cells at steady state and during disease and argue for a multilayered organization of the immune system on the basis of a spatiotemporal division of labour.


Assuntos
Sistema Imunitário , Imunidade Inata , Linfócitos , Animais , Camundongos , Asma/genética , Asma/imunologia , Asma/patologia , Modelos Animais de Doenças , Eosinófilos/patologia , Imunidade Inata/imunologia , Linfócitos/classificação , Linfócitos/imunologia , Proteínas de Fluorescência Verde , Sistema Imunitário/citologia , Sistema Imunitário/imunologia , Sistema Imunitário/patologia
5.
J Allergy Clin Immunol ; 152(6): 1619-1633.e11, 2023 12.
Artigo em Inglês | MEDLINE | ID: mdl-37659505

RESUMO

BACKGROUND: Chronic granulomatous disease (CGD) is caused by defects in any 1 of the 6 subunits forming the nicotinamide adenine dinucleotide phosphate oxidase complex 2 (NOX2), leading to severely reduced or absent phagocyte-derived reactive oxygen species production. Almost 50% of patients with CGD have inflammatory bowel disease (CGD-IBD). While conventional IBD therapies can treat CGD-IBD, their benefits must be weighed against the risk of infection. Understanding the impact of NOX2 defects on the intestinal microbiota may lead to the identification of novel CGD-IBD treatments. OBJECTIVE: We sought to identify microbiome and metabolome signatures that can distinguish individuals with CGD and CGD-IBD. METHODS: We conducted a cross-sectional observational study of 79 patients with CGD, 8 pathogenic variant carriers, and 19 healthy controls followed at the National Institutes of Health Clinical Center. We profiled the intestinal microbiome (amplicon sequencing) and stool metabolome, and validated our findings in a second cohort of 36 patients with CGD recruited through the Primary Immune Deficiency Treatment Consortium. RESULTS: We identified distinct intestinal microbiome and metabolome profiles in patients with CGD compared to healthy individuals. We observed enrichment for Erysipelatoclostridium spp, Sellimonas spp, and Lachnoclostridium spp in CGD stool samples. Despite differences in bacterial alpha and beta diversity between the 2 cohorts, several taxa correlated significantly between both cohorts. We further demonstrated that patients with CGD-IBD have a distinct microbiome and metabolome profile compared to patients without CGD-IBD. CONCLUSION: Intestinal microbiome and metabolome signatures distinguished patients with CGD and CGD-IBD, and identified potential biomarkers and therapeutic targets.


Assuntos
Microbioma Gastrointestinal , Doença Granulomatosa Crônica , Doenças Inflamatórias Intestinais , Humanos , Doença Granulomatosa Crônica/genética , NADPH Oxidases , Estudos Transversais
6.
Proc Natl Acad Sci U S A ; 108(2): 810-5, 2011 Jan 11.
Artigo em Inglês | MEDLINE | ID: mdl-21187377

RESUMO

Bacterial pathogens have evolved sophisticated signal transduction systems to coordinately control the expression of virulence determinants. For example, the human pathogen Vibrio cholerae is able to respond to host environmental signals by activating transcriptional regulatory cascades. The host signals that stimulate V. cholerae virulence gene expression, however, are still poorly understood. Previous proteomic studies indicated that the ambient oxygen concentration plays a role in V. cholerae virulence gene expression. In this study, we found that under oxygen-limiting conditions, an environment similar to the intestines, V. cholerae virulence genes are highly expressed. We show that anaerobiosis enhances dimerization and activity of AphB, a transcriptional activator that is required for the expression of the key virulence regulator TcpP, which leads to the activation of virulence factor production. We further show that one of the three cysteine residues in AphB, C(235), is critical for oxygen responsiveness, as the AphB(C235S) mutant can activate virulence genes under aerobic conditions in vivo and can bind to tcpP promoters in the absence of reducing agents in vitro. Mass spectrometry analysis suggests that under aerobic conditions, AphB is modified at the C(235) residue. This modification is reversible between oxygen-rich aquatic environments and oxygen-limited human hosts, suggesting that V. cholerae may use a thiol-based switch mechanism to sense intestinal signals and activate virulence.


Assuntos
Proteínas de Bactérias/metabolismo , Regulação Bacteriana da Expressão Gênica , Compostos de Sulfidrila/química , Transativadores/metabolismo , Vibrio cholerae/genética , Anaerobiose , Cisteína/genética , Perfilação da Expressão Gênica , Mutação , Oxigênio/química , Regiões Promotoras Genéticas , Proteômica , Transcrição Gênica , Ativação Transcricional , Vibrio cholerae/patogenicidade , Virulência
7.
Microbiology (Reading) ; 157(Pt 6): 1620-1628, 2011 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-21393367

RESUMO

The human pathogen Vibrio cholerae uses quorum sensing to regulate the expression of a number of phenotypes, including virulence factor production, in response to changes in cell density. It produces small molecules called autoinducers that increase in concentration as cell density increases, and these autoinducers bind to membrane sensors once they reach a certain threshold. This binding leads to signalling through a downstream phosphorelay pathway to alter the expression of the transcriptional regulator HapR. Previously, it was shown that the VarS/VarA two-component system acts on a component of the phosphorelay pathway upstream of HapR to regulate HapR expression levels. Here, we show that in addition to this mechanism of regulation, VarS and VarA also indirectly modulate HapR protein activity. This modulation is mediated by the small RNA CsrB but is independent of the known quorum-sensing system that links the autoinducers to HapR. Thus, the VarS/VarA two-component system intersects with the quorum-sensing network at two levels. In both cases, the effect of VarS and VarA on quorum sensing is dependent on the Csr small RNAs, which regulate carbon metabolism, suggesting that V. cholerae may integrate nutrient status and cell density sensory inputs to tailor its gene expression profile more precisely to surrounding conditions.


Assuntos
Proteínas de Bactérias/metabolismo , Regulação Bacteriana da Expressão Gênica , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Proteínas Quinases/metabolismo , Percepção de Quorum/genética , Transativadores/metabolismo , Vibrio cholerae/crescimento & desenvolvimento , Proteínas de Bactérias/genética , Meios de Cultura , Elementos de DNA Transponíveis/genética , Humanos , Peptídeos e Proteínas de Sinalização Intracelular/genética , Mutagênese Insercional , Proteínas Quinases/genética , Percepção de Quorum/fisiologia , RNA Longo não Codificante , RNA não Traduzido/genética , RNA não Traduzido/metabolismo , Transdução de Sinais , Transativadores/genética , Vibrio cholerae/genética , Vibrio cholerae/metabolismo
8.
Nucleic Acids Res ; 37(8): 2747-56, 2009 May.
Artigo em Inglês | MEDLINE | ID: mdl-19276207

RESUMO

The quorum-sensing pathway in Vibrio cholerae controls the expression of the master regulator HapR, which in turn regulates several important processes such as virulence factor production and biofilm formation. While HapR is known to control several important phenotypes, there are only a few target genes known to be transcriptionally regulated by HapR. In this work, we combine bioinformatic analysis with experimental validation to discover a set of novel direct targets of HapR. Our results provide evidence for two distinct binding motifs for HapR-regulated genes in V. cholerae. The first binding motif is similar to the motifs recently discovered for orthologs of HapR in V. harveyi and V. vulnificus. However, our results demonstrate that this binding motif can be of variable length in V. cholerae. The second binding motif shares common elements with the first motif, but is of fixed length and lacks dyad symmetry at the ends. The contributions of different bases to HapR binding for this second motif were demonstrated using systematic mutagenesis experiments. The current analysis presents an approach for systematically expanding our knowledge of the quorum-sensing regulon in V. cholerae and other related bacteria.


Assuntos
Proteínas de Bactérias/metabolismo , Regulação Bacteriana da Expressão Gênica , Percepção de Quorum/genética , Fatores de Transcrição/metabolismo , Vibrio cholerae/genética , Sequência de Bases , Sítios de Ligação , Sequência Consenso , DNA Bacteriano/química , Regiões Promotoras Genéticas , Proteínas Repressoras/metabolismo , Alinhamento de Sequência , Análise de Sequência de DNA , Transativadores/metabolismo , Vibrio cholerae/metabolismo
9.
Microbiome ; 9(1): 215, 2021 11 03.
Artigo em Inglês | MEDLINE | ID: mdl-34732258

RESUMO

BACKGROUND: The gut microbiome is altered in patients with inflammatory bowel disease, yet how these alterations contribute to intestinal inflammation is poorly understood. Murine models have demonstrated the importance of the microbiome in colitis since colitis fails to develop in many genetically susceptible animal models when re-derived into germ-free environments. We have previously shown that Wiskott-Aldrich syndrome protein (WASP)-deficient mice (Was-/-) develop spontaneous colitis, similar to human patients with loss-of-function mutations in WAS. Furthermore, we showed that the development of colitis in Was-/- mice is Helicobacter dependent. Here, we utilized a reductionist model coupled with multi-omics approaches to study the role of host-microbe interactions in intestinal inflammation. RESULTS: Was-/- mice colonized with both altered Schaedler flora (ASF) and Helicobacter developed colitis, while those colonized with either ASF or Helicobacter alone did not. In Was-/- mice, Helicobacter relative abundance was positively correlated with fecal lipocalin-2 (LCN2), a marker of intestinal inflammation. In contrast, WT mice colonized with ASF and Helicobacter were free of inflammation and strikingly, Helicobacter relative abundance was negatively correlated with LCN2. In Was-/- colons, bacteria breach the mucus layer, and the mucosal relative abundance of ASF457 Mucispirillum schaedleri was positively correlated with fecal LCN2. Meta-transcriptomic analyses revealed that ASF457 had higher expression of genes predicted to enhance fitness and immunogenicity in Was-/- compared to WT mice. In contrast, ASF519 Parabacteroides goldsteinii's relative abundance was negatively correlated with LCN2 in Was-/- mice, and transcriptional analyses showed lower expression of genes predicted to facilitate stress adaptation by ASF519 in Was-/-compared to WT mice. CONCLUSIONS: These studies indicate that the effect of a microbe on the immune system can be context dependent, with the same bacteria eliciting a tolerogenic response under homeostatic conditions but promoting inflammation in immune-dysregulated hosts. Furthermore, in inflamed environments, some bacteria up-regulate genes that enhance their fitness and immunogenicity, while other bacteria are less able to adapt and decrease in abundance. These findings highlight the importance of studying host-microbe interactions in different contexts and considering how the transcriptional profile and fitness of bacteria may change in different hosts when developing microbiota-based therapeutics. Video abstract.


Assuntos
Colite , Helicobacter , Animais , Colite/microbiologia , Modelos Animais de Doenças , Helicobacter/genética , Interações entre Hospedeiro e Microrganismos , Humanos , Inflamação , Camundongos
10.
Infect Immun ; 78(1): 461-7, 2010 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-19858311

RESUMO

Recent work has shown that in addition to cholera toxin (CT) and the toxin-coregulated pilus (TCP), other cytotoxic proteins in Vibrio cholerae also cause disease symptoms, and this is particularly evident in strains lacking CT. One such protein is the hemolysin encoded by hlyA. Here we show that, like CT and TCP, HlyA is repressed by the quorum-sensing-regulated transcription factor HapR. This repression occurs on two levels: one at the transcriptional level that is independent of the metalloprotease HapA and one at the posttranslational level that is mediated by HapA. The transcriptional regulation is significantly more apparent on solid media than in liquid cultures. This is the first time that hemolysis has been shown to be directly regulated by quorum sensing in V. cholerae, and it is interesting that, like other virulence factors, HlyA is also repressed by HapR, which is expressed late in infection.


Assuntos
Proteínas de Bactérias/metabolismo , Regulação Bacteriana da Expressão Gênica/fisiologia , Proteínas Hemolisinas/metabolismo , Processamento de Proteína Pós-Traducional/fisiologia , Percepção de Quorum/fisiologia , Transcrição Gênica/fisiologia , Vibrio cholerae/metabolismo , Proteínas de Bactérias/genética , Proteínas Hemolisinas/genética
11.
Biochim Biophys Acta ; 1792(4): 329-40, 2009 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-19245831

RESUMO

Telomeres play critical roles in protecting genome stability, and their dysfunction contributes to cancer and age-related degenerative diseases. The precise architecture of telomeres, including their single-stranded 3' overhangs, bound proteins, and ability to form unusual secondary structures such as t-loops, is central to their function and thus requires careful processing by diverse factors. Furthermore, telomeres provide unique challenges to the DNA replication and recombination machinery, and are particularly suited for extension by the telomerase reverse transcriptase. Helicases use the energy from NTP hydrolysis to track along DNA and disrupt base pairing. Here we review current findings concerning how helicases modulate several aspects of telomere form and function.


Assuntos
Envelhecimento/metabolismo , DNA Helicases/metabolismo , Replicação do DNA , Instabilidade Genômica , Neoplasias/enzimologia , Telômero/metabolismo , Envelhecimento/patologia , Animais , Humanos , Neoplasias/patologia , Recombinação Genética , Telomerase/metabolismo , Telômero/patologia
12.
Mol Microbiol ; 73(3): 507-17, 2009 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-19602148

RESUMO

Rhizobia form symbiotic nodules on host legumes and fix nitrogen for their hosts in exchange for nutrients. In order to establish this mutually beneficial relationship, rhizobia must compete with other soil bacteria in the host legume rhizosphere to colonize plant roots efficiently. A promoter-trap transposon screen in Mesorhizobium tianshanense, a Rhizobium that forms nodules on licorice (Glycyrrhiza uralensis) plants revealed that the expression of msiA, which encodes a putative exporter protein belonging to the LysE family of translocators, is activated by both legume exudates and MsiR, a LysR family transcriptional regulator. Chemical analysis suggests that the msiA-inducing signal in exudates is canavanine, an anti-metabolite present in the seeds and exudates of a variety of legume plants. We show that MsiA serves as a canavanine exporter that is indispensable for canavanine resistance in M. tianshanense. We also show that the expression of MsiA homologues in other rhizobial species is induced by canavanine and is critical for canavanine resistance. Furthermore, rhizobial canavanine resistance is important for root hair adherence as well as for survival in a canavanine-producing legume rhizosphere. Together, these data suggest that host legumes may exude specific antimetabolites into their surroundings to optimize the bacterial population in order to have successful symbiotic events with rhizobia.


Assuntos
Proteínas de Bactérias/metabolismo , Canavanina/metabolismo , Glycyrrhiza uralensis/metabolismo , Rhizobiaceae/genética , Simbiose , Proteínas de Bactérias/genética , Elementos de DNA Transponíveis , Regulação Bacteriana da Expressão Gênica , Genes Bacterianos , Glycyrrhiza uralensis/microbiologia , Rhizobiaceae/metabolismo , Nódulos Radiculares de Plantas/metabolismo , Nódulos Radiculares de Plantas/microbiologia , Sementes/metabolismo , Transdução de Sinais , Microbiologia do Solo
13.
Gut Microbes ; 11(5): 1139-1142, 2020 09 02.
Artigo em Inglês | MEDLINE | ID: mdl-32329652

RESUMO

User-friendly computational tools for 16S ribosomal RNA (rRNA) sequencing analysis enable researchers who are not bioinformaticians to analyze and interpret sequencing data from microbial communities. These tools' easy-to-use interfaces belie the sophisticated and rapidly-evolving science of their underlying algorithms. When analyzing 16S data from a simple microbiome experiment, we found that superficially unimportant decisions about the bioinformatic pipeline led to results with radically different biological interpretations. We share these results as a cautionary tale whose moral is that, in 16S analysis, the devil is in the details. Wet bench researchers should therefore strongly consider partnering with bioinformaticians or computational biologists when analyzing 16S data.


Assuntos
Algoritmos , Bactérias/classificação , Bactérias/genética , Microbioma Gastrointestinal/genética , RNA Ribossômico 16S/genética , Análise de Sequência de DNA , Animais , Biologia Computacional , DNA Bacteriano/genética , Genes de RNAr , Helicobacter/classificação , Helicobacter/genética , Camundongos
14.
Commun Integr Biol ; 1(1): 42-4, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-19704787

RESUMO

Pathogenic bacteria, such as Vibrio cholerae, must be capable of adapting to diverse living conditions, especially when transitioning from life in environmental reservoirs to life in a host. The abilities to sense arrival at a site suitable for colonization or infection and to respond with appropriate alterations in gene expression are crucial for a pathogen's success. Recently, we have shown that V. cholerae is able to recognize that it has reached its colonization site in the small intestine by sensing breakage of its flagellum as it penetrates the mucosal layer overlaying the intestinal epithelium. Flagellar loss results in the release of the anti-sigma factor FlgM and subsequent activation of the alternative sigma-factor FliA. FliA represses the quorum sensing-controlled transcriptional regulator, HapR, allowing increased expression of virulence factors such as Cholera Toxin (CT) and the Toxin Coregulated Pilus (TCP). In this way, the de-repression of virulence factor expression coincides with the arrival of bacteria at the site of infection at the intestinal mucosa. Our work reveals an interesting interplay between motility and quorum sensing signaling pathways to precisely time virulence gene expression during colonization.

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