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Legionella pneumophila

ABSTRACT: Legionella pneumophila subspecies

PROVIDER: PRJNA376177 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5831910_1.fastq.gz	Fastqsanger.gz
	SRR5831910_2.fastq.gz	Fastqsanger.gz
	SRR5831901_1.fastq.gz	Fastqsanger.gz
	SRR5831901_2.fastq.gz	Fastqsanger.gz
	SRR5831911_1.fastq.gz	Fastqsanger.gz

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Legionella pneumophila transcriptome during intracellular multiplication in human macrophages

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.

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Strand specific sequencing illustrates the complex transcriptional response of Legionella pneumophila during infection

Project description:Legionella pneumophila is a Gram-negative facultative intracellular human pathogen with a distinct biphasic lifestyle. One of its primary environmental hosts in the free-living amoeba Acanthamoeba castellanii and its infection by L. pneumophila mimics that seen in human macrophages. Here we present analysis of strand specific sequencing of the transcriptional response of L. pneumophila in broth growth and in infection of A. castellanii.

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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

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