Sus scrofa
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ABSTRACT:
PROVIDER: PRJNA97969 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from non-infected and Salmonella Choleraesuis infected mesenteric lymph nodes
| PRJNA97971 | ENA
Project description:Regulatory role of microRNAs in mesenteric lymph nodes after Salmonella Typhimurium infection
| PRJNA392048 | ENA
Project description:A first generation Affymetrix GeneChip® Porcine genome array was used to profile the gene expression in porcine mesenteric lymph nodes over a time course of infection with S. Typhimurium, including the acute (8 hours post inoculation (hpi), 24 hpi, 48 hpi) and chronic (21 days post-inoculation (dpi)) stages of infection. Our objectives were to 1) identify and examine the stereotypical gene expression response within host MLN to S. Typhimurium infection, 2) characterize global host responses by revealing the specific features of the hostâs innate immunity pathways, and 3) explore if and how S. Typhimurium may escape the host immune response and develop into a carrier state. Our study has attempted to investigate the features of host gene expression profiling during S. Typhimurium infection at the acute and chronic infection stages and to explore the mechanism by which S. Typhimurium can escape from the host immune response and develop a carrier state in the host. In conclusion, by using the Affymetrix porcine GeneChip, 848 differentially expressed genes were identified in porcine MLN during infection and several specific features of host response were revealed by gene cluster and pathway analysis. Our data are the first report to investigate global host responses to S. Typhimurium in porcine MLN, and this new study provides data applicable for studying enteric salmonellosis of pigs, as well as humans. Experiment Overall Design: Fifteen piglets from Salmonella spp.-free sows were weaned at 10 days (d) of age, shipped to the National Animal Disease Center, Ames, IA and raised in isolation facilities. To confirm that all piglets were free of Salmonella spp. prior to challenge, bacteriological cultures were performed on rectal swabs twice. Seven week old pigs were randomly divided into 2 groups, 3 non-infected pigs and 12 infected pigs. Three non-infected control pigs were necropsied 2 days prior to experimental infection. On day 0, pigs in the infected groups were intranasally challenged with 1 billion CFU of Salmonella enterica serovar Typhimurium. Three infected pigs were necropsied at 8 hours post-inoculation (hpi), 24 hpi, 48 hpi and 21 days post-inoculation (dpi). Tissue samples from the mesenteric lymph nodes (MLN) were collected and immediately frozen in liquid nitrogen for RNA isolation.
2008-06-15 | E-GEOD-7313 | biostudies-arrayexpress
Project description:To understand the host transcriptional response to S. enterica serovar Choleraesuis (S. Choleraesuis), the first generation Affymetrix porcine GeneChip® was used to identify differentially expressed genes in the mesenteric lymph nodes responding to infection at acute (8 hours (h), 24h, 48h post-inoculation (pi)) and chronic stages (21 days (d) pi); The objectives of this study were to identify and examine the stereotypical gene expression response within the host mesenteric lymph nodes to S. Choleraesuis infection, and to characterize the global host responses by revealing the specific features of the hostâs innate immunity. Experiment Overall Design: Fifteen piglets from Salmonella spp.-free sows were weaned at 10 days (d) of age, shipped to the National Animal Disease Center, Ames, IA and raised in isolation facilities. To confirm that all piglets were free of Salmonella spp. prior to challenge, bacteriological cultures were performed on rectal swabs twice. Seven week old pigs were randomly divided into 2 groups, 3 non-infected pigs and 12 infected pigs. Three non-infected control pigs were necropsied 3 days prior to experimental infection. On day 0, pigs in the infected groups were intranasally challenged with 1 billion CFU of Salmonella enterica serotype Choleraesuis x3246. Three infected pigs were necropsied at 8 hours post-inoculation (hpi), 24 hpi, 48 hpi and 21 day post-inoculation (dpi). Tissue samples from the mesenteric lymph nodes (MLN) were collected and immediately frozen in liquid nitrogen for RNA isolation.
2008-06-15 | E-GEOD-7314 | biostudies-arrayexpress
Project description:Salmonella enterica serotype Typhimurium cause a localized enteric infection in immunocompetent patients while human immunodeficiency virus (HIV)-infected patients develop a life threatening bacteremia. We used a rhesus macaque ileal loop model to study how simian immunodeficiency virus (SIV) infection triggers defects in mucosal barrier function that enhance S. Typhimurium dissemination. SIV infection resulted in significant depletion of CD4+ T cells in the intestinal mucosa. Gene expression profiling revealed a defective TH17 response (with suppression of IL-17 and IL-22 expression) and impaired homeostasis of the intestinal epithelium in SIV-infected animals during NTS infection. These findings correlated with an impaired ability of lamina propria CD4+ T cells from SIV-infected macaques to produce IL-17 upon ex vivo stimulation, while production of IFNï§ was not affected. This cytokine imbalance in SIV-infected animals was associated with reduced expression of genes required for intestinal epithelial maintenance and repair, increased fluid secretion during NTS infection, epithelial damage and translocation of a non-invasive S. Typhimurium mutant. Although no defects in neutrophil recruitment were noted, the ileum of SIV-infected animals contained lower levels of the enzyme myeloperoxidase, which may indicate defects in neutrophil killing capacity. S. Typhimurium was recovered in markedly increased numbers from the mesenteric lymph nodes of SIV-infected macaques, illustrating the increased potential for systemic dissemination during co-infection. Our data suggest that SIV-infection causes a multi-factorial defect in mucosal barrier function that promotes bacterial dissemination. Keywords: Disease state analysis Comparison of ileal gene expression profiles in SIV infected rhesus macaques in response to Salmonella challange.
2010-05-26 | E-GEOD-10567 | biostudies-arrayexpress
Project description:Expression data of ileal Peyer's patches from Salmonella Typhimurium infected pigs
| PRJNA394238 | ENA
Project description:Sus scrofa neutrophils infected by Salmonella Typhimurium
| PRJNA881236 | ENA
Project description:Expression data from mediastinal lymph nodes of piglets experimentally infected with porcine circovirus type 2 (PCV2)
| PRJNA114339 | ENA
Project description:Salmonella enterica serotype Typhimurium cause a localized enteric infection in immunocompetent patients while human immunodeficiency virus (HIV)-infected patients develop a life threatening bacteremia. We used a rhesus macaque ileal loop model to study how simian immunodeficiency virus (SIV) infection triggers defects in mucosal barrier function that enhance S. Typhimurium dissemination. SIV infection resulted in significant depletion of CD4+ T cells in the intestinal mucosa. Gene expression profiling revealed a defective TH17 response (with suppression of IL-17 and IL-22 expression) and impaired homeostasis of the intestinal epithelium in SIV-infected animals during NTS infection. These findings correlated with an impaired ability of lamina propria CD4+ T cells from SIV-infected macaques to produce IL-17 upon ex vivo stimulation, while production of IFN-gamma was not affected. This cytokine imbalance in SIV-infected animals was associated with reduced expression of genes required for intestinal epithelial maintenance and repair, increased fluid secretion during NTS infection, epithelial damage and translocation of a non-invasive S. Typhimurium mutant. Although no defects in neutrophil recruitment were noted, the ileum of SIV-infected animals contained lower levels of the enzyme myeloperoxidase, which may indicate defects in neutrophil killing capacity. S. Typhimurium was recovered in markedly increased numbers from the mesenteric lymph nodes of SIV-infected macaques, illustrating the increased potential for systemic dissemination during co-infection. Our data suggest that SIV-infection causes a multi-factorial defect in mucosal barrier function that promotes bacterial dissemination. Keywords: Disease state analysis
2008-02-21 | GSE10567 | GEO