Regulatory T cell-mediated resolution of lung injury: Identification of potential target genes via expression profiling
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE17355 | GEO | 2009/12/31
SECONDARY ACCESSION(S): PRJNA119073
REPOSITORIES: GEO
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Project description:We examined early and late gene expression changes using the IT LPS model of Acute Lung Injury (ALI). In this model, injury peaks at day 4 and is almost completely resolved by day 10 in wild type (WT) C57BL/6 mice. In contrast to the pattern in WT mice, lymphocyte-deficient Rag-1 -/- mice exhibit strikingly delayed resolution despite similar initial injury. Total RNA was isolated from mouse lung at time 0, 1, 4, and 10 days following LPS treatment of wild type and Rag-1 null mice using TRIzol reagent (Invitrogen Life Technologies), then purified using RNAeasy columns (Qiagen) with DNase I treatment according to the manufacturerâ??s recommendations. The quality of RNA was assessed using an Agilent 2100 Bioanalyzer (Agilent Technologies).
2010-06-24 | E-GEOD-17355 | biostudies-arrayexpress
Project description:Previous work has led us to examine the differences in the choroid plexus function in B10.pl WT mice versus B10.PL RAG-/- mice. We believe that there is a difference between those that are normal functioning and those that are lymphocyte deficient. To determine the gene expression profile of the choroid plexus in wild type mice as compared to those that are lymphocyte deficient. We hypothesize that there is altered expression in the genes that mediate cellular adhesion in choroid plexus from wild type mice as compared to those that are lymphocyte deficient. 8-10 week old animals (age and sex matched) were injected with Evan's blue post anesthetization. After waiting an hour the animals were euthanized and their brains were extracted and placed in RNALater for 24 hours. The brains were then sliced sagitally Keywords: RAG mutant, choroid plexus
2008-05-17 | GSE11443 | GEO
Project description:We have previously demonstrated that pre-B-cell colony enhancing factor (PBEF) ais a biomarker in sepsis and sepsis-induced acute lung injury (ALI) with genetic variants conferring ALI susceptibility118. In the current study, we explored the mechanistic participation of PBEF in ALI and ventilator-induced associated lung injury (VIALI). Initial in vitro studies and demonstrated rhPBEF aas a direct rat neutrophil chemotactic factor in vitro producing marked in vivo increases in BAL leukocytes (PMNs) in vivo following (intratracheal injection (,IT) in C57B6 mice. These latter changes were accompanied by increased BAL levels of the PMN chemoattractants (, KC and MIP2), and modest changes in lung vascular and but were not associated with significant increasesin alveolar permeability. We next explored the potential synergism between rhPBEF administration (IT) and a mechanical ventilation model of modest VILI lung injury (4 hours, 30 ml/kg tidal volume). We and observed dramatic synergistic increases in BAL PMNs, and both BAL protein and cytokine levels (IL-6, TNF-?, KC). Gene expression profiling Microarray analysis further supported a major role for PBEF in the induction of gene modules associated with ALI and VALI (NFkB pathway, leukocyte extravasation, apoptosis, toll receptor signaling). Finally, we exposed wild type and heterozygous PBEF+/- mice (targeted deletion of a single PBEF allele deletion) to a model of severe VILImechanical ventilation-induced lung injury (4 hours, 40 ml/kg tidal volume). PBEF+/- mice were significantly protected from VIALI-associated increases in BAL protein and BAL IL-6 levels and exhibited significantly reduced expression of ALI-associated gene expression modules. Together, these results indicate that PBEF is a key inflammatory mediator intimately involved in both the development and severity of ventilator-induced ALI. Experiment Overall Design: animals were treated by PBS, rhPBEF (IT administration), VILI (4 hours, 30 ml/kg tidal volume), or both.
2008-06-16 | E-GEOD-9314 | biostudies-arrayexpress
Project description:We have previously demonstrated that pre-B-cell colony enhancing factor (PBEF) ais a biomarker in sepsis and sepsis-induced acute lung injury (ALI) with genetic variants conferring ALI susceptibility118. In the current study, we explored the mechanistic participation of PBEF in ALI and ventilator-induced associated lung injury (VIALI). Initial in vitro studies and demonstrated rhPBEF aas a direct rat neutrophil chemotactic factor in vitro producing marked in vivo increases in BAL leukocytes (PMNs) in vivo following (intratracheal injection (,IT) in C57B6 mice. These latter changes were accompanied by increased BAL levels of the PMN chemoattractants (, KC and MIP2), and modest changes in lung vascular and but were not associated with significant increasesin alveolar permeability. We next explored the potential synergism between rhPBEF administration (IT) and a mechanical ventilation model of modest VILI lung injury (4 hours, 30 ml/kg tidal volume). We and observed dramatic synergistic increases in BAL PMNs, and both BAL protein and cytokine levels (IL-6, TNF-?, KC). Gene expression profiling Microarray analysis further supported a major role for PBEF in the induction of gene modules associated with ALI and VALI (NFkB pathway, leukocyte extravasation, apoptosis, toll receptor signaling). Finally, we exposed wild type and heterozygous PBEF+/- mice (targeted deletion of a single PBEF allele deletion) to a model of severe VILImechanical ventilation-induced lung injury (4 hours, 40 ml/kg tidal volume). PBEF+/- mice were significantly protected from VIALI-associated increases in BAL protein and BAL IL-6 levels and exhibited significantly reduced expression of ALI-associated gene expression modules. Together, these results indicate that PBEF is a key inflammatory mediator intimately involved in both the development and severity of ventilator-induced ALI. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Experiment Overall Design: animals were treated by PBS, rhPBEF (IT administration), VILI (4 hours, 30 ml/kg tidal volume), or both.
2008-06-16 | E-GEOD-9368 | biostudies-arrayexpress
Project description:Inflammation resolution is critical for sepsis induced acute lung injury (ALI) recovery. Interleukin-36 receptor (IL-36R) is a potent anti-inflammatory factor. However, its role in ALI resolution remains unclear. We investigated the effects of IL-36R during the ALI resolution process in a murine cecal ligation and puncture (CLP)-induced ALI model. Knockout IL-36R signaling aggravates CLP-induced lung injury, as manifested by elevated bacterial load and increased neutrophils recruitment to the lung. Thereafter, we used IL-36R knockout mice to discern the source cell of IL-36R during ALI. We found that IL-36R is predominantly generated by epithelial cells during the ALI process. Furthermore, we sorted lung epithelial cells on the ALI process. IL-36R-specific loss in epithelial cells leads to apoptosis through NF-κB pathway. Together, our findings identify molecules that are likely involved in sepsis induced lung injury that may inform biomarker and therapeutic development.
2024-01-02 | GSE240924 | GEO
Project description:Nasal epithelial cells of PCD and non-PCD patients grown at air-liquid interface for RNAseq analysis. A total of 10 non-PCD patients (ALI day 14), 9 non-PCD patients (ALI day 21), 8 non-PCD patients (ALI day 28), 4 PCD patients (ALI day 14, day 21 and day 28), and 23 PCD patients (ALI day 21). Non-PCD patients and the 4 PCD patients on the three ALI days were sequenced at a depth of 100M reads, the remaining 23 PCD patients were sequenced at a depth of 70M. Overall sequencing design was rRNA depletion and 150bp paired-end.
| EGAD00001009498 | EGA
Project description:Purpose: Acute lung injury (ALI) is a severe clinical disorder characterized by diffused capillary-alveolar barrier damage and noncardiogenic lung edema induced by excessive inflammation reactions. Nogo-B, a member of the reticulon 4 protein family, plays a critical role in modulating macrophages and neutrophils’ function in inflammation. Its role in ALI remains unclear. Methods: Pulmonary expression of Nogo-B was investigated in a LPS-induced ALI mice model. The effects and the underline mechanisms of Nogo-B expression on the severity of lung injury was assessed using histological examination, Bronchoalveolar lavage fluid (BALF) protein and inflammatory cells and cytokines measurement, and microarray analysis. Results: Nogo-B was normally highly expressed in the lungs of naïve C57BL/6 mice. Intra-tracheal instillation of LPS significantly repressed the Nogo-B expression in lung tissues and BALF cells of ALI mice. In addition, over-expression of pulmonary Nogo-B using an adenovirus vector which expresses a Nogo-B-RFP-3-flag fusion protein (Ad-Nogo-B) significantly prolonged the survival time of mice challenged with lethal dose of LPS. Histological results and BALF protein measurement convinced that Ad-Nogo-B treated mice had less severity of lung injury and alveolar protein exudation, as compared with control adenovirus treated mice (Ad-RFP). They also had higher MCP-1 secretion and alveolar macrophages infiltration, but lower neutrophils infiltration. Finally, using microarray analysis, we identified a protective gene, PTX3, was highly elevated in Ad-Nogo-B treated mice. Conclusions: Nogo-B played a protective role in LPS-induced ALI, which might exert its role through modulation of inflammatory response and PTX3 secretion. A total of 12 samples from mice treated with or without LPS in the presence of Ad-Nogo-B or Ad-RFP transfection (n=3 for each group)
2013-07-12 | E-GEOD-48787 | biostudies-arrayexpress
Project description:Children have a lower incidence and mortality from acute lung injury than adults, and infections are the most common event associated with acute lung injury (ALI). To study the effects of age on susceptibility to ALI, we investigated the responses to microbial products combined with mechanical ventilation in juvenile (21 day) and adult (16 week-old) mice. We hypothesized that the increased incidence and severity of lung injury associated with increasing age is due in large part to acquired changes in the way in which inflammatory responses are activated in the lungs in response to microbial products and mechanical ventilation.
2009-11-23 | GSE18341 | GEO
Project description:Purpose: To analyze the transcriptome difference of ILC2s isoalted from WT and RAG-/- mice under inflammaed condition Method: Lung ILC2s from mice chronically challenged with papain (40 µg/20 µl PBS, 6 subsequest papain challenges, day 0, 1, 2, 13, 14, and 15)
2023-01-11 | GSE166779 | GEO
Project description:Endothelial cells (ECs) serve as a semipermeable barrier and play a key role in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). It is well known that fibroblast growth factor receptor 1 (FGFR1) is a requirement for maintaining vascular integrity. However, how endothelial FGFR1 exerts its function remains obscure in ALI/ARDS. Here, we performed RNA-seq analysis to investigate transcriptional changes of ECs between saline and LPS group, WT (Fgfr1loxp/loxp) and endothelial Fgfr1-conditional knock out mice (Fgfr1iΔEC/iΔEC mice).
2023-03-29 | GSE216635 | GEO