Project description:Transcriptional profiling of macrophages derived from immune-selected (phagocytosis, complement activity in the alternative pathway, and antibody response after vaccination with swine erysipelas) in comparison with those from normal pigs
Project description:Female and male pigs were studied. Half of the pigs were exposed to immune activation from virally-infected mothers, and half were not exposed. At 60 days of age about one third of the pigs were given metabolic distress (fasting), one third of the pigs were given immune distress (poly(I:C)), and one third of the pigs were given Saline (control).
Project description:In this study, we show that the host response to DENV1-4 infection in immunocompetent mice recapitulates transcriptional and immunological changes that have been described in human studies. Dengue virus (DENV), a Flavivirus, causes a broad spectrum of disease in humans with key clinical signs including thrombocytopenia, vascular leakage and hemorrhaging. A major obstacle to understanding DENV immunity has been the lack of a validated immune-competent mouse model. Here, we report the infection profiles of human clinical isolates of DENV serotypes 1-4 in an immune-competent mouse model. We detected replicating DENV in the peritoneal cells, liver and the spleen that was generally resolved within 2 weeks. The DENV target cell types for infection were monocytes/macrophages, dendritic cells, endothelial cells, and we identified a novel DENV cellular target, fibroblast reticular cells of the spleen. We observed gross pathologies in the spleen and liver that are consistent with dengue disease, including hemorrhaging as well as transcriptional patterns suggesting that antiviral responses and tissue damage were induced. Key clinical blood parameters that define human DENV disease such as hemoconcentration, leukopenia and reduced number of platelets were also observed. Thus, immune-competent mice sustain replicating infection and experience signs, such as hemorrhaging, that define DENV disease in humans. This study thoroughly characterizes DENV1-4 infection in immune-competent mice and confirms the wild-type mouse model as a valid and reproducible system for investigating the mechanisms of DENV pathogenesis.
Project description:In this study, we show that the host response to DENV1-4 infection in immunocompetent mice recapitulates transcriptional and immunological changes that have been described in human studies. Dengue virus (DENV), a Flavivirus, causes a broad spectrum of disease in humans with key clinical signs including thrombocytopenia, vascular leakage and hemorrhaging. A major obstacle to understanding DENV immunity has been the lack of a validated immune-competent mouse model. Here, we report the infection profiles of human clinical isolates of DENV serotypes 1-4 in an immune-competent mouse model. We detected replicating DENV in the peritoneal cells, liver and the spleen that was generally resolved within 2 weeks. The DENV target cell types for infection were monocytes/macrophages, dendritic cells, endothelial cells, and we identified a novel DENV cellular target, fibroblast reticular cells of the spleen. We observed gross pathologies in the spleen and liver that are consistent with dengue disease, including hemorrhaging as well as transcriptional patterns suggesting that antiviral responses and tissue damage were induced. Key clinical blood parameters that define human DENV disease such as hemoconcentration, leukopenia and reduced number of platelets were also observed. Thus, immune-competent mice sustain replicating infection and experience signs, such as hemorrhaging, that define DENV disease in humans. This study thoroughly characterizes DENV1-4 infection in immune-competent mice and confirms the wild-type mouse model as a valid and reproducible system for investigating the mechanisms of DENV pathogenesis.
Project description:We describe the transcriptomic recall response to African swine fever virus (ASFV) upon in vitro stimulation in porcine peripheral blood mononuclear cells (PBMC) obtained three weeks after receiving an intranasal dose of 106 pfu of the live attenuated BA71ΔCD2 vaccine prototype. PBMC from 4 unvaccinated and 4 vaccinated pigs were stimulated with BA71ΔCD2 or left untreated for 10 hours, RNA was extracted, and bulk RNA-sequencing was performed. Major transcriptional changes were found in BA71ΔCD2-stimulated samples from vaccinated pigs. Indeed, compared to unvaccinated control pigs, cells from vaccinated animals showed an upregulation of genes corresponding to a robust Th1 response. Together with this adaptive immune response, we also distinguished an innate immune response characterized by the expression of macrophage-related inflammatory genes. Altogether, our results demonstrate that intranasal vaccination of pigs with BA71ΔCD2 induce a systemic Th1 memory response that is concomitant with a rapid enhancement of innate immunity upon in vitro activation.
Project description:Porcine reproductive and respiratory disease (PRRS) is the most important disease in swine industry worldwide. However, strategies such as vaccination and good biosecurity are not consistently successful to eliminate PRRSV. Though some interesting pathways have been tentatively examined recently, host molecular pathways utilized by PRRSV and the protective immune responses in resistant to PRRSV are largely unknown. In order to answer these questions, we herein characterize changes in global gene expressions in multiple tissues [tonsil, tracheobronchial lymph nodes (TBLN), Cranial lung (CR Lung), and distal lung (D Lung)] in response to PRRSV of high and low virulence. Both vaccinated and unvaccinated pigs are used for this study. Based on Ingenuity Pathway Analysis (IPA), molecule bases of some “black boxes” underlying immune responses are further identified. Our results indicate that cross talks among these pathways and immune balances/competition between host and virus are always happened during the pathogenesis of PRRS. connected loop design was used to accommodate samples from 4 treatment groups.
Project description:Microarray analysis of gene expression in 2-cell embryos obtained from developmentally competent MII oocytes or developmentally incompetent MII (NSN) oocytes. In this study we have compared the expression profile of 2-cell embryos obtained after following in vitro fertilisation of developmentally competent (control) or incompetent (NSN) MII oocytes with the aim of identifying the gene expression networks that operate at this specific stage of development.
Project description:To elucidate further molecular mechanisms underlying the regulation of hypoxia-adaptive phenotypes in Tibetan pigs, we used transcriptome microarrays from lung tissues of Tibetan pigs and Duroc pigs both at high and low altitude analyzed differentially expressed genes (DEGs), biological pathway and constructed co-expression regulation network. A total of 3,068 DEGs were identified which involved metabolic process, cellular process, immune biological process and angiogenesis pathway. The regulatory (RIF) and phenotypic (PIF) impact factors analysis identified several known and potentially regulators of hypoxia adaption, including IKBKG, KLF6 and RBPJ (RIF1), SF3B1, EFEMP1, HOXB6 and ATF6 (RIF2).
Project description:Intramuscular (i.m.) fat content influencing consumerâs acceptability of pork is considered as a limiting factor for meat quality. To gain insight into the biological basis of individual variability in i.m. fat content, both gene expression profiling and proteomic investigation were associated in pig longissimus muscle (LM). Keywords: intramuscular fat, gene expression, pigs, proteomics, microarray, pork meat Animals were sampled from a population of 1,000 pigs generated as an F2 intercross between two production sire lines: FH016 (Pietrain type, France Hybrides SA, St Jean de Braye, France) and FH019 (Synthetic line, from Duroc, Hampshire and Large White founders, France Hybrides SA, St Jean de Braye, France).
Project description:To gain insight into the role of testosterone in modulating hepatic fat accumulation, we collected liver tissues from high fat diet-fed intact male pigs, castrated male pigs, and castrated male pigs with testosterone replacement. RNA-Seq was employed to profile hepatic gene expression in pigs with different testosterone levels.