Transcriptomic analysis of lung epithelial cells after LPS inhalation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA735521 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14743462.fastq.gz | Fastqsanger.gz | |||
| SRR14743463.fastq.gz | Fastqsanger.gz | |||
| SRR14743464.fastq.gz | Fastqsanger.gz | |||
| SRR14743465.fastq.gz | Fastqsanger.gz | |||
| SRR14743466.fastq.gz | Fastqsanger.gz |
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Project description:Lung ECs express low levels of MHC-I at their surface. These levels are modestly increase 96h after LPS inhalation. At the transcriptional level, AT1, AT2 and Bronchiolar ECs highly increase the expression of MHC-I coding transcripts that reach level as high as mTECs. The amount of transcripts coding for Tap1, Tap2, Psmb8, Psmb9 and Psmb10 stay low compare to mTECs and seems limiting for an efficient surface expression of MHC-I in these three types of lung ECs.
2021-12-10 | GSE176228 | GEO
Project description:Analysis of transcriptional profile of lung resident macrophages during acute and resolution phase of LPS inhalation induced lung injury. Because macrophages coordinate both the induction and resolution of inflammatory lung injury, we examined the transcriptional signatures of resident lung macrophages isolated from LysM-GFP mice during baseline (0h), peak of injury (4h), and during the resolution phase (24h).
2021-10-01 | GSE174532 | GEO
Project description:Background: There are no highly effective medications for treating pneumonia. Ginseng and its derivatives have anti-inflammatory properties, but their unstable physicochemical and metabolic properties prevent them from being used to treat pneumonia. The aforementioned issues may be resolved by inhalation, but the precise mechanism of action must be investigated. Methods: In order to study the effects and mechanisms of PD inhalation drug delivery, models of LPS-induced murine holistic pneumonia, isolated macrophage inflammation, and epithelial cell co-culture are utilized. For the evaluation of efficacy, pathology and molecular assays have been utilized. Mechanisms of action and targets were screened and validated by molecular means using transcriptome sequencing. Efficacy and mechanism of action were ultimately validated using human BALF cell models. Also studied were pharmacokinetic parameters of inhaled PD. Results: Inhalation of PD dose-dependently reduced LPS-induced lung inflammation in mice, including inflammatory cell infiltration, lung histopathology, and inflammatory factor expression. Oral PD had the same anti-inflammatory effect as inhalation, but inhalation was more effective at the same dose. It could be a result of its increased bioavailability and improved pharmacokinetic parameters. Using transcriptome analysis and validation of macrophage and epithelial cell experiments, we discovered that PD may inhibit TNFA/TFNAR and IL7/IL7R signaling to inhibit macrophage inflammatory factor-induced epithelial cell apoptosis and promote value-added initiation. Human alveolar lavage cell experimentation confirmed this result. Conclusion: PD inhalation alleviates lung inflammation and pathology by inhibiting TNFA/TFNAR and IL7/IL7R signaling. PD may be a novel drug for the clinical treatment of lung inflammation.
2024-02-02 | GSE227089 | GEO
Project description:Acute lung inflammation can alter the pulmonary function of susceptible individuals and exacerbate the pathogenesis of chronic inflammatory lung diseases including chronic obstructive pulmonary disease (COPD), cystic fibrosis and asthma. Exposure to lipopolysaccharide (LPS) or endotoxin, a constituent of outer cell membrane of gram negative bacteria, induces airway inflammation that is primarily characterized by increased polymorphonuclear neutrophils (PMNs) at early time points. Because LPS is present in variety of occupational and home environments and is an active constituent of cigarette smoke it is a risk factor for increasing prevalence and severity of non-occupational COPD, for adult onset of asthma and for wheezing in children. In airway epithelial cells, LPS stimulation increases mucin gene expression and mucous production. Hypersecretion of mucus overwhelms the ciliary clearance and obstructs airways, causing morbidity and mortality in chronic inflammatory respiratory lung diseases. In addition, acute bacterial infection contributes to the exacerbation of chronic airway diseases, specifically in advanced COPD and CF subjects, leading to increased healthcare burden and higher mortality. Bcl-2, a prosurvival protein that inhibits cell death plays a key role in normal cellular homeostasis and regulates the integrity of the mitochondrial and endoplasmic reticulum membranes. Gain- and loss-of-function studies showed that Bcl-2 expression sustains hyperplastic epithelial cells, and Bcl-2 expression is elevated in airway epithelial cells of subjects with cystic fibrosis and asthma. The present study investigated which inflammatory mediators induce mucous cell metaplasia and Bcl-2 expression following LPS exposure. Microarray analyses of mRNA from airway epithelial cells captured by laser microdissection from rat lungs snap-frozen at day 0 and 2 post LPS exposure were analyzed. Microarray analysis of mRNA from airway epithelial cells captured by laser microdissection from rat lungs snap-frozen at day 0 and day 2 post LPS exposure was performed to identify inflammatory mediators modulated by LPS exposure. Specific pathogen-free F344/NCrR male rats of 8–10 wk of age (from NCI, Frederick, MD) were exposed to LPS (1000 ug in 0.5 ML Saline) and rats were sacrificed on day 0 and day 2 of LPS exposure. Right lungs were snap-frozen in OCT and airway epithelial cells were captured by laser-dissection microsopy to extract RNA. Gene expression data from nonexposed rats (0d) was used a control.
2012-03-01 | E-GEOD-36174 | biostudies-arrayexpress
Project description:Acute lung inflammation can alter the pulmonary function of susceptible individuals and exacerbate the pathogenesis of chronic inflammatory lung diseases including chronic obstructive pulmonary disease (COPD), cystic fibrosis and asthma. Exposure to lipopolysaccharide (LPS) or endotoxin, a constituent of outer cell membrane of gram negative bacteria, induces airway inflammation that is primarily characterized by increased polymorphonuclear neutrophils (PMNs) at early time points. Because LPS is present in variety of occupational and home environments and is an active constituent of cigarette smoke it is a risk factor for increasing prevalence and severity of non-occupational COPD, for adult onset of asthma and for wheezing in children. In airway epithelial cells, LPS stimulation increases mucin gene expression and mucous production. Hypersecretion of mucus overwhelms the ciliary clearance and obstructs airways, causing morbidity and mortality in chronic inflammatory respiratory lung diseases. In addition, acute bacterial infection contributes to the exacerbation of chronic airway diseases, specifically in advanced COPD and CF subjects, leading to increased healthcare burden and higher mortality. Bcl-2, a prosurvival protein that inhibits cell death plays a key role in normal cellular homeostasis and regulates the integrity of the mitochondrial and endoplasmic reticulum membranes. Gain- and loss-of-function studies showed that Bcl-2 expression sustains hyperplastic epithelial cells, and Bcl-2 expression is elevated in airway epithelial cells of subjects with cystic fibrosis and asthma. The present study investigated which inflammatory mediators induce mucous cell metaplasia and Bcl-2 expression following LPS exposure. Microarray analyses of mRNA from airway epithelial cells captured by laser microdissection from rat lungs snap-frozen at day 0 and 2 post LPS exposure were analyzed. Microarray analysis of mRNA from airway epithelial cells captured by laser microdissection from rat lungs snap-frozen at day 0 and day 2 post LPS exposure was performed to identify inflammatory mediators modulated by LPS exposure.
2012-03-01 | GSE36174 | GEO
Project description:Smoke inhalation injury is the leading cause of mortality in patients with burns. Circular RNAs (circRNAs) are a class of endogenous noncoding RNAs implicated in various diseases. However, their specific involvement in smoke inhalation injury remains poorly understood. High-throughput microarray analysis was used to identify differentially expressed circRNAs in plasma samples from patients with smoke inhalation injury compared to healthy controls. Five circRNAs were initially identified, and three were validated by quantitative real-time PCR (qRT-PCR). Bioinformatic analysis was used to establish circRNA–miRNA–mRNA networks. The predicted circRNA-miRNA-mRNA axes were further investigated in a rat inhalation injury model and in A549 cells. Microarray analysis revealed 65 differentially expressed circRNAs, of which three (hsa_circRNA_102928, hsa_circRNA_102059, and hsa_circRNA_101115) were confirmed by qRT-PCR, with one downregulated and two upregulated circRNAs. Bioinformatic analysis predicted 11 potential circRNA-microRNA-mRNA axes associated with smoke inhalation injury development, including the circRNA_102928/let-7f-2-3p/MDM1 axis. In a smoke inhalation injury rat model, the downregulation of circRNA_102928 and MDM1 mRNA, as well as the upregulation of let-7f-2-3p expression, coincided with prominent inflammation in the lungs. Overexpression of circRNA_102928 dramatically reduced let-7f-2-3p and significantly increased MDM1 mRNA levels in A549 cells. Furthermore, circRNA_102928 overexpression notably mitigated tumor necrosis factor-alpha and interleukin 1 beta expression and attenuated apoptosis in A549 cells. This study highlighted the role of the circRNA_102928/let-7f-2-3p/MDM1 axis in mediating lung inflammation and epithelial apoptosis in wood smoke inhalation injuries.
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Project description:Chronic LPS inhalation causes submucosal thickening and airway narrowing. To address the hypothesis that environmental airway disease is, in part, a fibroproliferative lung disease, we exposed C57BL/6 mice daily to LPS by inhalation for up to two months followed by one month of recovery. C57BL/6 mice exposed to daily inhaled LPS had significantly enhanced mRNA expression of TGF-beta1, TIMP-1, fibronectin-1, and pro-collagen types I, III, and IV and show prominent submucosal expression of the myofibroblast markers desmin and alpha-smooth muscle actin. To identify novel candidate genes that contribute to airway fibroproliferation, we performed microarray analysis on total lung RNA from mice exposed to LPS for one week. This analysis revealed a distinct subset of genes known to regulate ECM homeostasis. To further identify candidate genes specifically involved in generic fibroproliferation we interrogated this analysis with genes induced in C57BL/6 mouse lung by bleomycin. This analysis yielded a list of 212 genes in common. Prominent among which are genes know to be important in maintenance of bone homeostasis and which may play a central role in ECM homeostasis in the lung. These results suggest that there is a common subset of genes that regulate fibroproliferation in the lung independent of etiologic agent and site of injury. Keywords: mouse model of pulmonary fibrosis; timecourse
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Project description:LPS (10 μg/50 μl PBS; E. coli Serotype 055:B5, Sigma-Aldrich) was administered onto the nares. Baseline levels of genes in mice treated with vehicle (Hanks Balanced Salt solution (HBSS) and PBS), Intranasal S100s (10 μg/50 μl HBSS) were given 2 h before LPS; control mice received equal volumes of PBS and HBSS. Mice were sacrificed 4 h post LPS inhalation.
2016-08-01 | GSE74127 | GEO
Project description:Analysis of transcriptional profile of lung resident macrophages during acute and resolution phase of LPS inhalation induced lung injury.
| PRJNA730486 | ENA
Project description:Chronic LPS inhalation causes submucosal thickening and airway narrowing. To address the hypothesis that environmental airway disease is, in part, a fibroproliferative lung disease, we exposed C57BL/6 mice daily to LPS by inhalation for up to two months followed by one month of recovery. C57BL/6 mice exposed to daily inhaled LPS had significantly enhanced mRNA expression of TGF-ï¢1, TIMP-1, fibronectin-1, and pro-collagen types I, III, and IV and show prominent submucosal expression of the myofibroblast markers desmin and ï¡-smooth muscle actin. To identify novel candidate genes that contribute to airway fibroproliferation, we performed microarray analysis on total lung RNA from mice exposed to LPS for one week. This analysis revealed a distinct subset of genes known to regulate ECM homeostasis. To further identify candidate genes specifically involved in generic fibroproliferation we interrogated this analysis with genes induced in C57BL/6 mouse lung by bleomycin. This analysis yielded a list of 212 genes in common. Prominent among which are genes know to be important in maintenance of bone homeostasis and which may play a central role in ECM homeostasis in the lung. These results suggest that there is a common subset of genes that regulate fibroproliferation in the lung independent of etiologic agent and site of injury. Experiment Overall Design: 4 RNA pools of 3 animals each exposed to aerosolized LPS and 4 RNA pools of 3 animals each exposed to air only were co-hybridized with the Stratagene Universal Mouse Reference RNA. Each sample was assayed in duplicate with Cy3 and Cy5 dyes swapped. Experiment Overall Design:
2008-04-05 | E-GEOD-8566 | biostudies-arrayexpress