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Human Rhinovirus Infection of the Respiratory Tract Affects Sphingolipid Synthesis

ABSTRACT: Human Rhinovirus Infection of the Respiratory Tract Affects Sphingolipid Synthesis

PROVIDER: PRJNA781263 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16969917.fastq.gz	Fastqsanger.gz
	SRR16969918.fastq.gz	Fastqsanger.gz
	SRR16969919.fastq.gz	Fastqsanger.gz
	SRR16969920.fastq.gz	Fastqsanger.gz
	SRR16969921.fastq.gz	Fastqsanger.gz

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Human Rhinovirus Infection of the Respiratory Tract Affects Sphingolipid Synthesis

Project description:We report the application of bulk RNA sequencing to RNA extracted from lung tissue and magnetic bead isolated EpCAM+ lung epithelial cells and CD45+ lung immune cells from mice. Heterozygous serine palmitory transferase subunit 2 , Sptlc2+/- (SPT) and Sptlc2+/+ controls (WT) mice were included. Differential gene expression analysis reveals genes within the sphingolipid synthesis pathway are similarly expressed in the lung and lung epithelial cells of RV infected WT mice and SPT mice (both infected and uninfected).

2021-11-20 | GSE189056 | GEO

Human Rhinovirus Infection of the Respiratory Tract Affects Sphingolipid Synthesis.

Project description:The 17q21 asthma susceptibility locus includes asthma risk alleles associated with decreased sphingolipid synthesis, likely resulting from increased expression of ORMDL3. ORMDL3 inhibits serine-palmitoyl transferase (SPT), the rate-limiting enzyme of de novo sphingolipid synthesis. There is evidence that decreased sphingolipid synthesis is critical to asthma pathogenesis. Children with asthma and 17q21 asthma risk alleles display decreased sphingolipid synthesis in blood cells. Reduced SPT activity results in airway hyperreactivity, a hallmark feature of asthma. 17q21 asthma risk alleles are also linked to childhood infections with human rhinovirus (RV). This study evaluates the interaction of RV with the de novo sphingolipid synthesis pathway, and the alterative effects of concurrent SPT inhibition in SPT-deficient mice and human airway epithelial cells. In mice, RV infection shifted lung sphingolipid synthesis gene expression to a pattern that resembles genetic SPT deficiency, including decreased expression of Sptssa, a small SPT subunit. This pattern was pronounced in lung epithelial cellular adhesion molecule (EpCAM+) cells and reproduced in human bronchial epithelial cells. RV did not affect Sptssa expression in lung CD45+ immune cells. RV increased sphingolipids unique to the de novo synthesis pathway in mouse lung and human airway epithelial cells. Interestingly, these de novo sphingolipid species were reduced in the blood of RV-infected wild-type mice. RV exacerbated SPT deficiency-associated airway hyperreactivity. Airway inflammation was similar in RV-infected wild-type and SPT-deficient mice. This study reveals the effects of RV infection on the de novo sphingolipid synthesis pathway, elucidating a potential mechanistic link between 17q21 asthma risk alleles and rhinoviral infection.

| S-EPMC8937237 | biostudies-literature

Genome-wide analysis of whole blood transcriptional response to Respiratory Syncytial Virus, Influenza and Rhinovirus lower respiratory tract infection (LRTI) in children

Project description:Analysis of transcriptional profiles in whole blood from children < 2 years of age (and healthy matched controls) with RSV, rhinovirus and influenza infection. The hypothesis tested is that transcriptional profile heterogeneity will reflect patient clinical heterogeneity and that RSV infection induces a distinct host response compared with influenza and rhinovirus infection Total RNA extracted from whole blood (lysed in Tempus tubes) drawn from individual pediatric patients with acute RSV, influenza and Rhinovirus lower respiratory tract infection. A total of 241 samples are analyzed: 135 with acute RSV LRTI, 30 with Rhinovirus LRTI, 16 with influenza LRTI, 39 age-sex matched healthy controls and 21 samples obtained one month after the acute hospitalization in children with RSV. Samples GSM1226237-GSM1226272, which were hybridized to Platform GPL10558, were normalized separately from the other Samples in this Series, which were hybridized to Platform GPL6884. 'GSE38900_non-normalized_GSM1226237-GSM1226272.txt.gz' includes the non-normalized data for Samples GSM1226237-GSM1226272; 'GSE38900_non-normalized.txt.gz' includes the non-normalized data for the other Samples.

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Effects of inhibiting sphingolipid synthesis and TOR signaling on the Candida albicans transcriptome

Project description:Goal: We employed RNA-seq to detect changes in the transcriptome of the yeast Candida albicans in response to the addition of myriocin, a sphingolipid synthesis inhibitor, or caffeine, a drug that blocks the TOR kinase. The effects of the drugs were studied in wild-type cells and in the rtg3 mutant strain.

2019-04-01 | GSE125332 | GEO

Inhibiting sphingolipid synthesis improves outcomes and survival in GARP-mutant wobbler mouse, an ALS model

Project description:Defects of the endosomal and lysosomal systems have been increasingly linked to adult neurodegenerative diseases1,2. Deficiencies in the retrograde trafficking pathway between endosomes and the Golgi apparatus lead to forms of Alzheimer’s and Parkinson’s diseases in the case of retromer mutations, or to the rare progressive cerebello-cerebral atrophy type 2 (PCCA2) for mutations of the Golgi-associated retrograde protein (GARP) complex3. Mutations in GARP subunits lead to abnormal cellular lipid metabolism, with accumulation of sterol esters and sphingoid bases, and concomitant lysosomal dysfunction in yeast, murine, or human cells4,5. However, whether these lipid changes cause neurodegeneration and if so, which lipids are toxic, is unknown. Here, we show that GARP defects lead to global changes of cellular protein distribution, including missorting of numerous disease-linked enzymes of sphingolipid metabolism, and to the accumulation of sphingolipid intermediates in wobbler fibroblasts. Inhibiting sphingolipid synthesis in wobbler mice, a murine model of GARP deficiency with features of amyotrophic lateral sclerosis (ALS), improved wellness scores and grip strength, and increased lifespan. Our findings indicate that regulation of sphingolipids by the GARP complex is essential for neuronal health and suggest that inhibition of sphingolipid synthesis might provide a therapeutic strategy for treatment of neurodegenerative diseases due to defects in retrograde endosome-to-Golgi membrane trafficking.

2022-02-15 | PXD007981 | Pride

Rhinovirus C

Project description:Human rhinovirus C

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Effects of inhibiting sphingolipid synthesis and TOR signaling on the Candida albicans transcriptome

Project description:Effects of inhibiting sphingolipid synthesis and TOR signaling on the Candida albicans transcriptome

| PRJNA515877 | ENA

Proteomic and Phosphoproteomic Analyses of Yeast Reveal the Global Cellular Response to Sphingolipid Depletion

Project description:Sphingolipids are essential components of eukaryotic cells with important functions in membrane biology and cellular signaling. Their levels are tightly controlled and coordinated with the abundance of other membrane lipids. How sphingolipid homeostasis is achieved is not yet well understood. Studies performed primarily in yeast showed that the phosphorylation states of several enzymes and regulators of sphingolipid synthesis are important, although a global understanding for such regulation is lacking. Here, we used high-resolution mass-spectrometry-based proteomics and phosphoproteomics, in combination with data from a chemical genetic screen, to analyze the cellular response to sphingolipid synthesis inhibition. Our dataset reveals that changes in protein phosphorylation, rather than protein abundance, dominate the response to blocking sphingolipid synthesis. We identified Ypk1 signaling as a major pathway that is activated under these conditions, and we confirmed and identified Ypk1 targets. We also revealed key aspects of the cellular response to sphingolipid deprivation, including nodes that intersect with sterol metabolism and modification of lipid transport. Our data provide a rich resource for on-going mechanistic studies of key elements of the cellular response to the depletion of sphingolipid levels and the maintenance of sphingolipid homeostasis.

2016-12-23 | PXD003854 | Pride

Rhinovirus C

Project description:Human rhinovirus C overview

| PRJNA69715 | ENA

Genome-wide analysis of whole blood transcriptional response to Respiratory Syncytial Virus, Influenza and Rhinovirus lower respiratory tract infection (LRTI) in children

2013-11-12 | GSE38900 | GEO