Spectrométrie de masse

@article{normant_how_2022,

title = {How the Presence of Hemin Affects the Expression of the Different Iron Uptake Pathways in Pseudomonas aeruginosa Cells},

author = {Vincent Normant and Lauriane Kuhn and Mathilde Munier and Philippe Hammann and Gaëtan L. A. Mislin and Isabelle J. Schalk},

doi = {10.1021/acsinfecdis.1c00525},

issn = {2373-8227},

year  = {2022},

date = {2022-01-01},

journal = {ACS infectious diseases},

volume = {8},

number = {1},

pages = {183--196},

abstract = {Iron is an essential nutriment for almost all organisms, but this metal is poorly bioavailable. During infection, bacteria access iron from the host by importing either iron or heme. Pseudomonas aeruginosa, a gram-negative pathogen, secretes two siderophores, pyoverdine (PVD) and pyochelin (PCH), to access iron and is also able to use many siderophores produced by other microorganisms (called xenosiderophores). To access heme, P. aeruginosa uses three distinct uptake pathways, named Has, Phu, and Hxu. We previously showed that P. aeruginosa expresses the Has and Phu heme uptake systems and the PVD- and PCH-dependent iron uptake pathways in iron-restricted growth conditions, using proteomic and RT-qPCR approaches. Here, using the same approaches, we show that physiological concentrations of hemin in the bacterial growth medium result in the repression of the expression of the proteins of the PVD- and PCH-dependent iron uptake pathways, leading to less production of these two siderophores. This indicates that the pathogen adapts its phenotype to use hemin as an iron source rather than produce PVD and PCH to access iron. Moreover, the presence of both hemin and a xenosiderophore resulted in (i) the strong induction of the expression of the proteins of the added xenosiderophore uptake pathway, (ii) repression of the PVD- and PCH-dependent iron uptake pathways, and (iii) no effect on the expression levels of the Has, Phu, or Hxu systems, indicating that bacteria use both xenosiderophores and heme to access iron.},

keywords = {Hemin, hemin (heme) uptake, Iron, iron homeostasis, iron uptake, outer membrane transporters, PPSE, proteomics, Pseudomonas aeruginosa, siderophore, Siderophores},

pubstate = {published},

tppubtype = {article}

}

@article{gasser_esterase_2021,

title = {The Esterase PfeE, the Achilles' Heel in the Battle for Iron between Pseudomonas aeruginosa and Escherichia coli},

author = {Véronique Gasser and Lauriane Kuhn and Thibaut Hubert and Laurent Aussel and Philippe Hammann and Isabelle J. Schalk},

doi = {10.3390/ijms22062814},

issn = {1422-0067},

year  = {2021},

date = {2021-03-01},

urldate = {2021-03-01},

journal = {International Journal of Molecular Sciences},

volume = {22},

number = {6},

pages = {2814},

abstract = {Bacteria access iron, a key nutrient, by producing siderophores or using siderophores produced by other microorganisms. The pathogen Pseudomonas aeruginosa produces two siderophores but is also able to pirate enterobactin (ENT), the siderophore produced by Escherichia coli. ENT-Fe complexes are imported across the outer membrane of P. aeruginosa by the two outer membrane transporters PfeA and PirA. Iron is released from ENT in the P. aeruginosa periplasm by hydrolysis of ENT by the esterase PfeE. We show here that pfeE gene deletion renders P. aeruginosa unable to grow in the presence of ENT because it is unable to access iron via this siderophore. Two-species co-cultures under iron-restricted conditions show that P. aeruginosa strongly represses the growth of E. coli as long it is able to produce its own siderophores. Both strains are present in similar proportions in the culture as long as the siderophore-deficient P. aeruginosa strain is able to use ENT produced by E. coli to access iron. If pfeE is deleted, E. coli has the upper hand in the culture and P. aeruginosa growth is repressed. Overall, these data show that PfeE is the Achilles' heel of P. aeruginosa in communities with bacteria producing ENT.},

keywords = {Carrier Proteins, co-cultures, enterobactin, Escherichia coli, Escherichia coli Proteins, Esterases, Iron, iron homeostasis, iron uptake, outer membrane transporters, PPSE, Pseudomonas aeruginosa, siderophore, TonB},

pubstate = {published},

tppubtype = {article}

}

@article{S2018,

title = {Quorum-sensing regulator RhlR but not its autoinducer RhlI enables Pseudomonas to evade opsonization},

author = {Samantha Haller and Adrien Franchet and A Hakkim and J Chen and E Drenkard and S Yu and Steffi Schirmeier and Zi Li and Nelson Martins and FM Ausubel and Samuel Liégeois and Dominique Ferrandon},

url = {http://embor.embopress.org/content/early/2018/03/09/embr.201744880},

doi = {10.15252/embr.201744880},

year  = {2018},

date = {2018-03-09},

journal = {EMBO Reports},

keywords = {Drosophila, ferrandon, M3i, Opsonin Proteins, Phagocytosis, Pseudomonas aeruginosa, Quorum Sensing},

pubstate = {published},

tppubtype = {article}

}

@article{haller_assessing_2014b,

title = {Assessing Pseudomonas virulence with a nonmammalian host: Drosophila melanogaster},

author = {Samantha Haller and Stefanie Limmer and Dominique Ferrandon},

doi = {10.1007/978-1-4939-0473-0_56},

issn = {1940-6029},

year  = {2014},

date = {2014-01-01},

journal = {Methods Mol. Biol.},

volume = {1149},

pages = {723--740},

abstract = {Drosophila melanogaster flies represent an interesting model to study host-pathogen interactions as: (1) they are cheap and easy to raise rapidly and do not bring up ethical issues, (2) available genetic tools are highly sophisticated, for instance allowing tissue-specific alteration of gene expression, e.g., of immune genes, (3) they have a relatively complex organization, with distinct digestive tract and body cavity in which local or systemic infections, respectively, take place, (4) a medium throughput can be achieved in genetic screens, for instance looking for Pseudomonas aeruginosa mutants with altered virulence. We present here the techniques used to investigate host-pathogen relationships, namely the two major models of infections as well as the relevant parameters used to monitor the infection (survival, bacterial titer, induction of host immune response).},

keywords = {Animal, Animals, Antimicrobial Cationic Peptides, Biological Assay, Colony Count, Disease Models, ferrandon, Hemolymph, Host-Pathogen Interactions, M3i, Mammals, Microbial, Pseudomonas aeruginosa, Pseudomonas Infections, Reverse Transcriptase Polymerase Chain Reaction, Virulence},

pubstate = {published},

tppubtype = {article}

}

@article{limmer_pseudomonas_2011b,

title = {Pseudomonas aeruginosa RhlR is required to neutralize the cellular immune response in a Drosophila melanogaster oral infection model},

author = {Stefanie Limmer and Samantha Haller and Eliana Drenkard and Janice Lee and Shen Yu and Christine Kocks and Frederick M Ausubel and Dominique Ferrandon},

doi = {10.1073/pnas.1114907108},

issn = {1091-6490},

year  = {2011},

date = {2011-10-01},

journal = {Proc. Natl. Acad. Sci. U.S.A.},

volume = {108},

number = {42},

pages = {17378--17383},

abstract = {An in-depth mechanistic understanding of microbial infection necessitates a molecular dissection of host-pathogen relationships. Both Drosophila melanogaster and Pseudomonas aeruginosa have been intensively studied. Here, we analyze the infection of D. melanogaster by P. aeruginosa by using mutants in both host and pathogen. We show that orally ingested P. aeruginosa crosses the intestinal barrier and then proliferates in the hemolymph, thereby causing the infected flies to die of bacteremia. Host defenses against ingested P. aeruginosa included an immune deficiency (IMD) response in the intestinal epithelium, systemic Toll and IMD pathway responses, and a cellular immune response controlling bacteria in the hemocoel. Although the observed cellular and intestinal immune responses appeared to act throughout the course of the infection, there was a late onset of the systemic IMD and Toll responses. In this oral infection model, P. aeruginosa PA14 did not require its type III secretion system or other well-studied virulence factors such as the two-component response regulator GacA or the protease AprA for virulence. In contrast, the quorum-sensing transcription factor RhlR, but surprisingly not LasR, played a key role in counteracting the cellular immune response against PA14, possibly at an early stage when only a few bacteria are present in the hemocoel. These results illustrate the power of studying infection from the dual perspective of host and pathogen by revealing that RhlR plays a more complex role during pathogenesis than previously appreciated.},

keywords = {Animal, Animals, Bacteremia, Bacterial Proteins, Cellular, Disease Models, ferrandon, Genes, Genetically Modified, Hemolymph, Host-Pathogen Interactions, Immunity, Insect, M3i, Mutation, Oral, Pseudomonas aeruginosa, Pseudomonas Infections, Quorum Sensing, Trans-Activators, Viral, Virulence},

pubstate = {published},

tppubtype = {article}

}

@article{limmer_virulence_2011b,

title = {Virulence on the fly: Drosophila melanogaster as a model genetic organism to decipher host-pathogen interactions},

author = {Stefanie Limmer and Jessica Quintin and Charles Hetru and Dominique Ferrandon},

issn = {1873-5592},

year  = {2011},

date = {2011-06-01},

journal = {Curr Drug Targets},

volume = {12},

number = {7},

pages = {978--999},

abstract = {To gain an in-depth grasp of infectious processes one has to know the specific interactions between the virulence factors of the pathogen and the host defense mechanisms. A thorough understanding is crucial for identifying potential new drug targets and designing drugs against which the pathogens might not develop resistance easily. Model organisms are a useful tool for this endeavor, thanks to the power of their genetics. Drosophila melanogaster is widely used to study host-pathogen interactions. Its basal immune response is well understood and is briefly reviewed here. Considerations relevant to choosing an adequate infection model are discussed. This review then focuses mainly on infections with two categories of pathogens, the well-studied Gram-negative bacterium Pseudomonas aeruginosa and infections by fungi of medical interest. These examples provide an overview over the current knowledge on Drosophila-pathogen interactions and illustrate the approaches that can be used to study those interactions. We also discuss the usefulness and limits of Drosophila infection models for studying specific host-pathogen interactions and high-throughput drug screening.},

keywords = {Animal, Animals, Anti-Infective Agents, Disease Models, Drug Delivery Systems, Drug Design, Drug Resistance, ferrandon, Fungi, High-Throughput Screening Assays, Host-Pathogen Interactions, Humans, M3i, Microbial, Pseudomonas aeruginosa},

pubstate = {published},

tppubtype = {article}

}