Unknown,Transcriptomics,Genomics,Proteomics

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Temporal response of mouse peritoneal cells to a non-pathogenic E. coli infection

ABSTRACT: Analysis of early and late changes in the mouse peritoneal cells in response to E. coli induced sepis. Result provide an insight into the molecular function and pathways expressed at these different time points. The mice were divided in two groups; the first group of mice were not treated with E. coli and was referred to as the naive group. Each mouse of the second group was injected with 2 X108 cells of a non- pathogenic isolate of E. coli suspended in a phosphate buffered saline (PBS) solution. After 1h, 2h and 18h of E. coli administration, peritoneal lavage fluid was obtained from two mice each for E. coli treated group at 1 and 2h and three mice of both groups (control and E. coli treated) at 18h. A common naive group of 2 mice harvested at 2h served as a control for both 1h and 2h.

ORGANISM(S): Mus musculus

SUBMITTER: Minny Bhatty

PROVIDER: E-GEOD-34114 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Acute respiratory distress syndrome (ARDS) carries about a 50 percent mortality and is frequently associated with an infection (sepsis). Life-support treatment with mechanical ventilation rescues many patients, although superimposed infection or multiple organ failure can result in death. The outcome of a patient developing sepsis highly depends on the degree of pre-existing inflammation prior to the infection. In this study, we describe each stage of the inflammation process using a transcriptional approach and an animal model. Femelle C57BL6/J mice received an intraveinous oleic acid injection to induce an acute lung injury. PBMC expression patterns have been analyzed using a 9900 cDNA mouse microarray (MUSV29K). Our gene-expression analysis revealed marked changes in the immune and inflammatory response metabolic pathways, notably lipid metabolism and transcription. The early pro-inflammatory stage (1H-1H30) is characterized by the release of immune response and activation of inflammatory mechanisms. Later (3H-4H), the immune cells migrate into inflamed tissues through interaction with vascular endothelial cells. Finally, at late stages of lung inflammation (18H-24H), metabolism is deeply disturbed. Highly expressed pro-inflammatory cytokines activate transcription of many genes as well as lipid metabolism. This global overview of critical events occuring during lung inflammation is essential to understand infectious pathologies such as sepsis where inflammation and infection are interwined. From now on, it becomes possible to isolate the impact of a pathogen at the transcriptional level from the global gene expression modifications resulting from the infection associated with the inflammation. Also, our work allowed to identify genes involved in the response to inflammation. Among those, several may be potential target for gene therapy. Wild-type femelle C57Bl/6J mice, 7 weeks old, were obtained from Charles River and housed in a specific pathogen-free animal facility. We studied 39 mice divided into 6 groups. Each group was identified according to the incubation time: 1H, 1H30, 3H, 4H, 18H and 24H. The 1H group was made up of 6 mice (2 physiological serum and 4 OA); the 1H30 group was made up of 8 mice (2 physiological serum and 6 OA); the 3H group was made up of 7 mice (2 physiological serum and 5 OA); the 4H group was made up of 6 mice (2 physiological serum and 4 OA); the 18H group was made up of 6 mice (2 physiological serum and 4 OA); the 24H group was made up of 6 mice (2 physiological serum and 4 OA). Several RNA samples have been hybridized on 2 filters consisting in technical replicates. Data normalized by quantile without adjustment on physiological serum linked on Series record.

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Temporal response of mouse peritoneal cells to a non-pathogenic E. coli infection

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