Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA120629 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Large scale transcriptomic characterization of mice blood inflammation during Acute Lung Injury (PBMC)
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Project description:Large scale transcriptomic characterization of mice lung inflammation during Acute Lung Injury (lung)
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Project description:Large scale transcriptomic characterization of mice brain inflammation during Acute Lung Injury (brain)
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Project description:Innate immune cells control acute eosinophilic lung inflammation induced by cystein proteases. Here we characterize the dynamic change of gene expression profile in basophils, natural helper cells and eosinophils during lung inflammation via cystein protease Examination of mRNA levels in individual cell populations, basophils, natural helper cells and eosinophils of the lung from naïve mice and papain treated mice.
2014-03-28 | E-GEOD-56292 | biostudies-arrayexpress
Project description:Hypoxemia is a defining feature of acute respiratory distress syndrome (ARDS), an often-fatal complication of pulmonary or systemic inflammation, yet the resulting tissue hypoxia, and its impact on immune responses, is often neglected. Here we showed that ARDS patients were hypoxaemic and monocytopenic within the first 48 hours of ventilation. Monocytopenia was also observed in mouse models of acute lung injury, in which tissue hypoxia drove the suppression of type I interferon signalling in the bone marrow. This impaired monopoiesis, resulted in reduced accumulation of monocyte-derived macrophages and enhanced neutrophil-mediated inflammation in the lung. Administration of CSF1 in mice with hypoxic lung injury rescued the monocytopenia, altered the nature of circulating monocytes, increased monocyte-derived macrophages in the lung and limited injury. Thus, tissue hypoxia altered the dynamics of the immune response to the detriment of the host and interventions to address the aberrant response offer new therapeutic strategies for ARDS.
2022-08-12 | PXD033151 | Pride
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.
2011-06-01 | E-GEOD-19030 | biostudies-arrayexpress
Project description:Nogo-B protects mice against lipopolysaccharide-induced acute lung injury
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