Project description:ddMS2 run of mouse lung tissue and plasma extract using C8 column in 7.5-minute gradient and positive polarity mode in Q Exactive plus.
Project description:ddMS2 run of mouse lung tissue and plasma extract using C8 column in 7.5-minute gradient and positive polarity mode in Q Exactive plus.
Project description:apply C8 column and 7.5 minutes run to feces, small intestine and large intestine samples from mice under negative polarity mode in ddMS2.
Project description:Female and male C57BL/6J mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA) at 16 weeks age. Mice were intranasal infected with a sublethal does of 7.5×104 EID50 A/Puerto Rico/8/34 influenza virus (PR8; Charles River, Wilmington, MA, USA) or mock infected (naïve) with 1X PBS. After euthanasia at 7 days post infection lung and nasal septum were collected from animals to perform transcriptome analysis by RNA sequencing.
Project description:Recombinant human plasma gelsolin (rhu-pGSN) improves survival and reduces morbidity of mice infected with influenza. The goal of this study was to investigate the transcriptome profile of lung tissue from infected mice, treated with either rhu-pGSN or vehicle.
Project description:Periodic outbreaks of highly pathogenic avian H5N1 influenza viruses and the current H1N1 pandemic highlight the need for a more detailed understanding of influenza virus pathogenesis. To investigate the host transcriptional response induced by pathogenic influenza viruses, we used a functional-genomics approach to compare gene expression profiles in lungs from wild-type 129S6/SvEv and interferon receptor (IFNR) knockout mice infected with either the fully reconstructed H1N1 1918 pandemic virus (1918) or the highly pathogenic avian H5N1 virus Vietnam/1203/04 (VN/1203). Eight- to 10-week-old female wild-type and IFNR1-/- mice (on a 129S6/SvEv background) were anesthetized by intraperitoneal injection of 0.2 ml of 2,2,2-tribromoethanol in tert-amylalcohol (Avertin; Sigma-Aldrich, Milwaukee, WI). Ten times the 50% lethal dose (LD50), 3.2 × 10^4 PFU (1918) or 7 × 10^3 PFU (VN/1203), in 50 μl of infectious virus diluted in phosphate-buffered saline (PBS) was inoculated intranasally (i.n.). Lung tissue was harvested for microarray analysis from infected animals at 1, 3, and 4 days post-innoculation. For RNA isolation, lungs were frozen in individual tubes and stored in solution D (4 M guanidinium thiocyanate, 25 mM sodium citrate, 0.5% sarcosyl, 0.1 M β-mercaptoethanol). Separate microarrays were run for each infected mouse. This included 2 animals/time point for 1918 virus-infected mice (24 animals total) or 3 animals/time point for VN/1203-infected mice (36 animals total). Lung tissue from three uninfected wild type 129S6/SvEv mice was collected as a mock control. Equal masses of total RNA from the lung tissue of the three mice were pooled prior to being run on microarray. Two-channel microarrays were used to determine gene expression in the lungs. For each individual infected lung, gene expression from an infected lung was compared to gene expression from the pooled RNA from the mock control.
Project description:To examine reaction in lung residential cells to influenza viral infection, lung epithelial cells (AEC), clara cells, DC, Mast cells, macrophages, eosinophil, and neutrophils were isolated from lung of mice infected with influenza viruses at 3 day postinfection.
Project description:We evaluated the effects of maoto, a traditional kampo medicine, as a herbal multi-compound medicine on host transcriptome responses in a mouse model of influenza infection. On the fifth day of oral administration to mice intranasally infected with influenza virus (A/PR/8/34 (H1N1), maoto significantly improved survival rate, decreased viral titer, and ameliorated the infection-induced phenotype as compared with control mice. Analysis of the lung and plasma transcriptome profile showed that maoto significantly up-regulated the expression of macrophage- and T-cell-related genes. Collectively, these results suggest that maoto regulates the host’s inflammatory response.