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ABSTRACT: Second generation sequencing results of Haemophilus parasuis

PROVIDER: PRJNA898583 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22221526_1.fastq.gz	Fastqsanger.gz
	SRR22221526_2.fastq.gz	Fastqsanger.gz
	SRR22221527_1.fastq.gz	Fastqsanger.gz
	SRR22221527_2.fastq.gz	Fastqsanger.gz
	SRR22221528_1.fastq.gz	Fastqsanger.gz

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Expression data from Porcine alveolar macrophages infection with Haemophilus parasuis (HPS)

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Expression data from Porcine alveolar macrophages of piglets experimentally infected with Haemophilus parasuis serotype 4 (HPS4) for 28 days

Project description:Porcine alveolar macrophages (PAMs) play impoartant role in innate immunity. Haemophilus parasuis is the etiological agent of Glasser’s disease in pigs. Haemophilus parasuis is the etiological agent of Glasser’s disease in pigs. We used microarrays to study the transcriptome of PAMs infection with HPS4.

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Expression data from Porcine alveolar macrophages infection with Haemophilus parasuis (HPS)

Project description:Porcine alveolar macrophages (PAMs) play impoartant role in innate immunity. Haemophilus parasuis is the etiological agent of Glasser’s disease in pigs. We used microarrays to study the transcriptome of PAMs infection with Haemophilus parasuis. Healthy Pigs were intratracheally challenged with H.parasuis strain 0165. And the PAMs were isolated at 6 dpi. RNA extraction were extracted from PAMs that obtained from infection pigs and control pigs and hybridization on Affymetrix microarrays. We sought to obtain the differently expressed genes that related to H.parasuis infection to understand the mechanism of PAMs against H.parasuis.

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Expression data from Porcine alveolar macrophages of piglets experimentally infected with Haemophilus parasuis serotype 4 (HPS4) for 28 days

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Comparison of Gene Expression in Lung of Pigs Exhibiting Different Susceptibilities to Glasser's Disease

Project description:Haemophilus parasuis is the causative agent of Glasser’s disease in pigs, but this bacterium is also routinely isolated from healthy animals. Whether colonization of the respiratory tract ultimately results in the onset of disease is determined by a combination of environmental, bacterial and host factors that are incompletely understood. This study used DNA microarrays to identify genes that were differentially expressed in the lung of colostrum deprived animals previously characterized as being either ‘Resistant’ or ‘Susceptible’ to infection by H. parasuis in a bacterial challenge experiment at either 24 or 72 hours post-inoculation. Gene expression profiles were obtained by comparing gene expression between each group and a pool of ‘Uninfected control’ animals. The aims of the experiment were: 1) To identify genes associated with resistance and susceptibility to H. parasuis. 2) To identify genes associated with the molecular pathology of Glasser's disease. 3) To identify genes involved in the host response to infection in the lung.

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Global Gene Expression Profiles of Cecropin B Induces Resistance in Haemophilus parasuis

Project description:To understand the mechanism of the adaptations, global gene expression profiles of the cecropin B--resistant strains of Haemophilus parasuis, The development of cecropin B (CB) resistance in H. parasuis SH0165 by exposing SH0165 using various concentrations of CB was investigated. One colony of bacterial cultures grown on TSA containing 30M-NM-<g/mL CB was named CBR30, CBR30 cultured in TSA without CB for 50 passages was named CBR30-50. we used microarray technology to analyze the variation of the H. parasuis SH0165 transcriptional profile in CBR30 and CBR30-50. Our analysis to identify several genes whose system could be involved in inorganic ion transport, amino acid transport, and metabolism. Quantitative PCR was used to validate the differential expression of selected genes. The H. parasuis SH0165 control group was normal culture with no tilmicosin at OD600 >0.3 (12 h). The H. parasuis CBR30 was normal culture with 30M-NM-<g/mL cecropin B at OD600 >0.3 (20 h). The H. parasuis CBR30-50 was normal culture with no cecropin B at OD600 >0.3 (12 h). Three independent experiments were performed on each group using a different sample for each experiment.

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