Legionella pneumophila subsp. pneumophila str. Philadelphia 1
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ABSTRACT:
PROVIDER: PRJNA386103 | ENA |
REPOSITORIES: ENA
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Project description:The CpxRA two-component system promotes intracellular survival and is a key regulator of virulence factors in Legionella pneumophila
| PRJNA298257 | ENA
Project description:The bacterium Legionella pneumophila is capable of intracellular replication within freshwater protozoa as well as human alveolar macrophages, the latter of which results in the serious pneumonia Legionnaires’ disease. A primary factor involved in these host cell interactions is the Dot/Icm Type IV secretion system that is responsible for translocating effector proteins needed to establish and maintain the bacterial replicative niche. Several regulatory factors have been identified to control the expression of the Dot/Icm system and effectors, one of which is the CpxRA two-component system, suggesting essentiality for virulence. However, studies elsewhere have shown that L. pneumophila strains harboring mutated cpxRA genes have minimal to no impact on L. pneumophila intracellular growth in protozoa and macrophages. In this study, we generated L. pneumophila cpxR, cpxA, and cpxRA in-frame null mutant strains to further delineate the role of the CpxRA system in bacterial survival and virulence. Surprisingly, we found that cpxR and cpxRA are essential for intracellular replication within Acanthamoeba castellanii, but not in U937 macrophage-like cells. Transcriptome analysis revealed that CpxRA regulates a large number of virulence-associated proteins including a number of Dot/Icm effectors as well as 14 Type II secreted substrates. Furthermore, the cpxR and cpxRA mutants were more sodium resistant than wildtype, and cpxRA expression reaches maximal levels during post-exponential phase. Taken together, our findings suggest the CpxRA system is a key contributor to L. pneumophila virulence via virulence factor regulation.
2016-09-16 | GSE73873 | GEO
Project description:Legionella pneumophila was exposed for 3h to 160 ug/ml of CuO nanoparticle. Untreated samples are used as the control condition.
2013-03-04 | GSE41966 | GEO
Project description:Legionella pneumophila is the causative agent of Legionnaires’ disease, an acute pulmonary infection. L. pneumophila is able to infect and multiply in both phagocytic protozoan, such as Acanthamoeba castellanii, and mammalian professional phagocytes. The best-known virulence determinant used by L. pneumophila to infect host cells is a Type IVb translocation system named Icm/Dot, which is used to modify the host cell functions to the benefit of the bacteria. To date the Icm/Dot systeme is known to translocate more than 100 effectors. While the transcriptional response of Legionella to the intracellular environement of A. castelannii as already been investigated, much less is known of how Legionella reacts transcriptionnally inside human macrophages. In this study, the transcriptome of L. pneumophila was monitored during exponential and post-exponential phase in rich AYE broth and during infection of human cultured macrophages by using microarray and a RNA amplification procedure called SCOTS to allow for the study of conditions of low bacterial loads. Among the genes induced intracellularly are those involved in amino acid synthesis pathway leading to L-arginine, L-histidne and L-proline as well as many transport system involved in amino acid and iron uptake. The Icm/Dot systems is not differentially expressed inside cells compare to the E phase control but the effectors are strongly induced. The intracellular transcriptome was further used to identify putative new Icm/Dot effectors and translocation was show to occur for 3 of them. This study provides a comprehensive view of how L. pneumophila react to the human macrophages intracellular environment.
2011-01-01 | GSE23029 | GEO
Project description:Abstract Legionella pneumophila, the causative agent of Legionnaire’s disease, grows within macrophages and manipulates target cell signaling. Formation of a Legionella-containing replication vacuole requires the function of the bacterial type IV secretion system (Dot/Icm), which transfers protein substrates into the host cell cytoplasm. A global microarray analysis was used to examine the response of human macrophage-like U937 cells to low dose infections with L. pneumophila. The most striking change in expression was the Dot/Icm-dependent up-regulation of anti-apoptotic genes positively controlled by the transcriptional regulator NF-?B. Consistent with this finding, L. pneumophila triggered nuclear localization of NF-?B in human and mouse macrophage in a Dot/Icm-dependent manner. The mechanism of activation at low dose infections involved a signaling pathway that occurred independently of the TLR adaptor MyD88, and cytoplasmic sensor Nod1. In contrast, high MOI conditions caused a host cell response that masked the unique Dot/Icm-dependent activation of NF-?B. Inhibition of NF-?B translocation into the nucleus resulted in premature host cell death and termination of bacterial replication. In the absence of one anti-apoptotic protein, PAI-2, host cell death increased in response to L. pneumophila infection, indicating that induction of anti-apoptotic genes is critical for host cell survival. Keywords: time course, dose response
2006-08-17 | GSE5551 | GEO
Project description:Legionella pneumophila subsp. pneumophila str. Philadelphia 1 Genome sequencing
| PRJNA195914 | ENA
Project description:Legionella pneumophila is a water-borne pathogen, and thus survival in the aquatic environment is central to its transmission to humans. Hence, identifying genes required for its survival in water could help prevent Legionnaires’ disease outbreaks. In the present study, we investigate for the first time the role of the sigma factor RpoS in promoting the survival in water, where L. pneumophila experiences total nutrient deprivation. The rpoS mutant showed a significant survival defect compared to the wild-type strain in defined water medium (DFM). Then, we analyzed the transcriptome of the rpoS mutant during exposure to water using whole genome microarray analysis. We found that RpoS negatively affects the expression of several genes, including genes required for replication, cell division, translation and transcription, suggesting that the mutant fails to shutdown major metabolic programs.
2014-12-04 | GSE56258 | GEO
Project description:Legionella pneumophila strain Philadelphia-1 Reannotation Project
| PRJNA292755 | ENA
Project description:Transcriptomic change of Legionella pneumophila in water.
| PRJNA268489 | ENA