About: Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung

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About: Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung
Creator	Fu, Panfeng Arbieva, Zarema Ebenezer, David Harijith, Anantha Hu, Hong Jung, Segun Krishnan, Yashaswin Madduri, Ravi Maienschein-Cline, Mark Natarajan, Viswanathan
Source	Medline; PMC
abstract	BACKGROUND: Pseudomonas aeruginosa (PA) is an opportunistic Gram-negative bacterium that causes serious life threatening and nosocomial infections including pneumonia. PA has the ability to alter host genome to facilitate its invasion, thus increasing the virulence of the organism. Sphingosine-1- phosphate (S1P), a bioactive lipid, is known to play a key role in facilitating infection. Sphingosine kinases (SPHK) 1&2 phosphorylate sphingosine to generate S1P in mammalian cells. We reported earlier that Sphk2(−/−) mice offered significant protection against lung inflammation, compared to wild type (WT) animals. Therefore, we profiled the differential expression of genes between the protected group of Sphk2(−/−) and the wild type controls to better understand the underlying protective mechanisms related to the Sphk2 deletion in lung inflammatory injury. Whole transcriptome shotgun sequencing (RNA-Seq) was performed on mouse lung tissue using NextSeq 500 sequencing system. RESULTS: Two-way analysis of variance (ANOVA) analysis was performed and differentially expressed genes following PA infection were identified using whole transcriptome of Sphk2(−/−) mice and their WT counterparts. Pathway (PW) enrichment analyses of the RNA seq data identified several signaling pathways that are likely to play a crucial role in pneumonia caused by PA such as those involved in: 1. Immune response to PA infection and NF-κB signal transduction; 2. PKC signal transduction; 3. Impact on epigenetic regulation; 4. Epithelial sodium channel pathway; 5. Mucin expression; and 6. Bacterial infection related pathways. Our genomic data suggests a potential role for SPHK2 in PA-induced pneumonia through elevated expression of inflammatory genes in lung tissue. Further, validation by RT-PCR on 10 differentially expressed genes showed 100% concordance in terms of vectoral changes as well as significant fold change. CONCLUSION: Using Sphk2(−/−) mice and differential gene expression analysis, we have shown here that S1P/SPHK2 signaling could play a key role in promoting PA pneumonia. The identified genes promote inflammation and suppress others that naturally inhibit inflammation and host defense. Thus, targeting SPHK2/S1P signaling in PA-induced lung inflammation could serve as a potential therapy to combat PA-induced pneumonia.
has issue date	2019-12-16(xsd:dateTime)
bibo:doi	10.1186/s12864-019-6367-9
bibo:pmid	31842752
has license	cc-by
sha1sum (hex)	52e083e335c8c29b8867ac67d5090b71348f2eac
schema:url	https://doi.org/10.1186/s12864-019-6367-9
resource representing a document's title	Genetic deletion of Sphk2 confers protection against Pseudomonas aeruginosa mediated differential expression of genes related to virulent infection and inflammation in mouse lung
has PubMed Central identifier	PMC6916461
has PubMed identifier	31842752
schema:publication	BMC Genomics
resource representing a document's body	covid:52e083e335c8c29b8867ac67d5090b71348f2eac#body_text
is schema:about of	named entity 'NF-' named entity 'VIRULENT' named entity 'SPHK2' named entity 'INFLAMMATION' named entity 'DIFFERENTIAL EXPRESSION' named entity 'ELEVATED' named entity 'IMMUNE RESPONSE' named entity 'KEY' named entity 'RESULTS' named entity 'NOSOCOMIAL INFECTIONS' named entity 'BACTERIAL INFECTION' named entity 'PATHWAYS' named entity 'ANIMALS' named entity '262' named entity 'USING' named entity 'SPHK2' named entity 'ENRICHMENT' named entity 'IDENTIFIED' named entity 'MUCIN' named entity 'RESPONSE TO' named entity 'LIKELY' named entity 'THEIR' named entity 'LUNG' named entity 'GENOMIC DATA' named entity 'SIGNALING PATHWAYS' named entity 'EXPRESSION' named entity 'LIFE THREATENING' named entity 'SPHINGOSINE' named entity 'PLAY' named entity 'BETTER' named entity 'TERMS' named entity 'POTENTIAL' named entity 'SPHINGOSINE-1-PHOSPHATE' named entity 'PATHWAY' named entity '100%' named entity 'CHANGES' named entity 'REGULATION' named entity 'ITS' named entity 'INCLUDING' named entity 'RELATED' named entity 'BIOACTIVE LIPID' named entity 'HOST' named entity 'FOLD CHANGE' named entity 'DELETION' named entity 'CONCORDANCE' named entity 'WHOLE TRANSCRIPTOME' named entity 'INVOLVED' named entity 'CELLS' named entity 'UNDERSTAND' named entity 'RELATED' named entity 'GENES' named entity 'MOUSE LUNG' named entity 'DELETION' named entity 'GENERATE' named entity 'EXPRESSED' named entity 'LUNG INFLAMMATION' named entity 'PSEUDOMONAS AERUGINOSA' named entity 'FOLLOWING' named entity 'SYSTEM' named entity 'GENOME' named entity 'CAUSES' named entity 'MICE' named entity 'DATA' covid:arg/52e083e335c8c29b8867ac67d5090b71348f2eac named entity 'SEQ' named entity 'TWO-WAY ANALYSIS OF VARIANCE' named entity 'INFECTION' named entity 'GENETIC' named entity 'PNEUMONIA' named entity 'MECHANISMS' named entity 'PSEUDOMONAS AERUGINOSA' named entity 'MEDIATED'

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