Analysis of transcriptional profile of lung resident macrophages during acute and resolution phase of LPS inhalation induced lung injury.
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ABSTRACT:
PROVIDER: PRJNA730486 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
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| SRR14566009.fastq.gz | Fastqsanger.gz | |||
| SRR14566010.fastq.gz | Fastqsanger.gz | |||
| SRR14566011.fastq.gz | Fastqsanger.gz |
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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).
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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.
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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: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:
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Project description:Acute respiratory distress syndrome (ARDS) is a serious lung failure with a high mortality rate and no effective pharmacological therapies. While the cellular and molecular mechanisms underlying the induction of ARDS have been extensively studied, those controlling its resolution remain poorly understood. Recent human cohort studies have implied the correlation between the severity of ARDS and the paucity of blood basophils. To examine the causative relationships between basophils and the pathogenesis of ARDS, we assessed the effect of basophil depletion in an LPS-induced mouse model of ARDS and explored the possible role for basophils in the induction and resolution of ARDS by using genetically engineered mice and single-cell RNA-sequencing (scRNA-seq) analyses. Intratracheal LPS administration induced severe lung inflammation with massive neutrophil accumulation, followed by the recovery to homeostatic conditions. Basophil depletion impaired the recovery but not induction of lung inflammation, demonstrating the crucial role for basophils in the resolution phase of ARDS. scRNA-seq analysis identified that basophils accumulating in the lung were predominant sources of cytokine IL-4. Mice with basophil-specific IL-4 deficiency failed to resolve the lung inflammation. This was also the case in mice with neutrophil-specific IL-4 receptor deficiency. scRNA-seq analysis suggested that basophil-derived IL-4 acts on neutrophils to suppress their expression of anti-apoptotic genes and pro-inflammatory mediators. Thus, the present study demonstrated that basophils play a crucial role in the resolution phase of a mouse model of ARDS through the production of IL-4 which in turn acts on neutrophils to restrict lung inflammation.
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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 environmental airway disease; chronic LPS exposure
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