Arginine sensing regulates virulence gene expression and disease progression in enteric pathogens.
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ABSTRACT:
PROVIDER: PRJEB35294 | ENA |
REPOSITORIES: ENA
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Project description:Disease outbreaks due to the consumption of legume seedlings contaminated with human enteric bacterial pathogens like Escherichia coli O157:H7 and Salmonella enterica are reported every year. We found surface and internal colonization of Medicago truncatula by Salmonella enterica and Escherichia coli O157:H7 even with inoculum levels as low as two bacteria per plant. Expression analyses using microarray revealed that some Medicago truncatula genes were regulated in a similar manner in response to both of these enteric pathogens.
2013-12-18 | GSE53406 | GEO
Project description:Abstract Protozoa of the genus Leishmania are the causative agents of leishmaniasis in humans. These parasites cycle between promastigotes in the sand fly mid-gut and amastigotes in phagolysosome of mammalian macrophages. During infection, they up-regulate host nitric oxide synthase and arginase expression, both of which use arginine as a substrate. These elevated activities deplete macrophage arginine pools, a situation that invading Leishmania must overcome since it is an essential amino acid. Leishmania donovani imports exogenous arginine via a mono-specific amino acid transporter (AAP3) and utilizes it primarily through the polyamine pathway to provide precursors for trypanothione biosynthesis. Here we report the discovery of a pathway whereby promastigote and amastigote forms of the Leishmania sense the lack of environmental arginine and respond with rapid up-regulation in AAP3 expression and activity, as well as several other transporters. Significantly, this arginine deprivation response is also activated in parasites during macrophage infection. Phosphoproteomic analyses of L. donovani promastigotes have implicated a mitogen activated protein kinase 2 (MPK2)-mediated signaling cascade in this response and L. mexicana mutants lacking MPK2 are unable to respond to arginine deprivation. In addition, these mutants cannot differentiate into amastigotes in axenic culture or in peritoneal macrophages, and fail to establish an infection in mice. We propose that sensing arginine levels plays a critical role in Leishmania virulence by activating a rapid metabolic reaction for salvaging this amino acid in response to the lower arginine concentration in the macrophage phagolysosome.
2016-04-11 | PXD002830 | Pride
Project description:Abstract Protozoa of the genus Leishmania are the causative agents of leishmaniasis in humans. These parasites cycle between promastigotes in the sand fly mid-gut and amastigotes in phagolysosome of mammalian macrophages. During infection, they up-regulate host nitric oxide synthase and arginase expression, both of which use arginine as a substrate. These elevated activities deplete macrophage arginine pools, a situation that invading Leishmania must overcome since it is an essential amino acid. Leishmania donovani imports exogenous arginine via a mono-specific amino acid transporter (AAP3) and utilizes it primarily through the polyamine pathway to provide precursors for trypanothione biosynthesis. Here we report the discovery of a pathway whereby promastigote and amastigote forms of the Leishmania sense the lack of environmental arginine and respond with rapid up-regulation in AAP3 expression and activity, as well as several other transporters. Significantly, this arginine deprivation response is also activated in parasites during macrophage infection. Phosphoproteomic analyses of L. donovani promastigotes have implicated a mitogen activated protein kinase 2 (MPK2)-mediated signaling cascade in this response and L. mexicana mutants lacking MPK2 are unable to respond to arginine deprivation. In addition, these mutants cannot differentiate into amastigotes in axenic culture or in peritoneal macrophages, and fail to establish an infection in mice. We propose that sensing arginine levels plays a critical role in Leishmania virulence by activating a rapid metabolic reaction for salvaging this amino acid in response to the lower arginine concentration in the macrophage phagolysosome.
2016-02-17 | PXD002766 | Pride
Project description:The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss and dysmotility during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via b2-adrenergic receptors (b2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemic production of interleukin (IL)-4 and -13 by eosinophils, which induced arginase-expressing MMs that prevented neuronal loss from an unrelated infection located in a different intestinal region. Collectively, these data suggest that distinct enteric pathogens trigger a state of disease- or tissue tolerance that preserves ENS number and functionality.
2021-08-17 | GSE182294 | GEO
Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell M-bM-^@M-^S to M-bM-^@M-^S cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes. Comparison of transcriptional regulation of enteropathogenic E. coli serotype O55:H7 wild type and the qseC mutant in the absence or presence of epinephrine signal to identify the regulated targets
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Project description:Enterococcus faecalis is a commensal bacterium in the gastrointestinal tract (GIT) of humans and other organisms. Outside of the GIT, E. faecalis can cause infections in root canals, wounds, surgical sites, the urinary tract, and on heart valves. Many of these infections can be polymicrobial, and a variety of toxins and nutritional signals influence interactions between E. faecalis and other microbes. Like other bacteria, E. faecalis metabolizes arginine through the arginine deiminase (ADI) pathway, which converts arginine to ornithine and releases ATP, ammonia, and CO2. E. faecalis arginine metabolism also affects virulence of other pathogens, such as Clostridioides difficile and Escherichia coli, during co-culture. E. faecalis may encounter elevated levels of arginine in the GIT or the oral cavity, where arginine is used as an additive in dental therapeutics to disrupt plaque formation and biofilm growth by oral streptococci. However, little is known about how E. faecalis responds to growth in arginine. To address this gap, we used RNAseq and additional in vitro assays to measure changes in growth, gene expression, and biofilm formation in arginine relative to control conditions. Here, we demonstrate that arginine decreases E. faecalis biofilm production and causes widespread differential expression of genes related to metabolism, nutrient transport, quorum sensing, and polysaccharide synthesis. Growth in arginine also increases aggregation of E. faecalis cultures and promotes decreased susceptibility to the antibiotics ampicillin and ceftriaxone. Together, this shows that E. faecalis undergoes global transcriptional changes during growth in arginine and provides a platform for better understanding of how the presence of arginine in the niches colonized by E. faecalis affects the physiology of this organism in addition to the virulence of surrounding microbes.
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