Project description:proteome of LPS-stimulated macrophages in Il18-knockout mouse' liver and lung. proteome of LPS-stimulated macrophages in widetype mouse' liver and lung.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways and the function of all RNAs in a certain functional state of a specific cell was studied, mainly including non-coding RNAs.The aim of this study was to compare lung tissue transcriptome analysis (RNA-SEQ) with microarray and quantitative reverse transcription polymerase chain reaction (QRT-PCR) methods for LPS-induced acute lung injury and to evaluate the optimal high-throughput data analysis protocol. Methods: LncRNA profiles of normal lung tissue and LPS-induced acute lung injury after 24h in mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000 Results: A total of 8,610 lncRNAs were identified in the normal and LPS groups. Conclusions: Our study represents detailed analysis of lung tissue transcriptomes, withh biological replicates, generated by RNA-seq technology. Novel ideas are presented to expand our knowledge on the regulation mechanisms of lncRNA-related ceRNAs in the pathogenesis of ALI.
Project description:Abstract Isorhynchophylline, a tetracyclic indole alkaloid, has anti-inflammatory and antioxidant activities against cardiovascular diseases and central nervous system disorders. Acute lung injury (ALI) is a manifestation of inflammation concentrated in the lungs and has a high incidence rate and mortality. Here, we established a mouse model of ALI and observed the effects of isorhynchophylline. Proteomic results showed that 5727 proteins were detected in mouse lung tissues, and 16 proteins were screened out. Isorhynchophylline could reverse the trend of these differential proteins. In addition, isorhynchophylline can act on integrin alpha M to reduce neutrophil recruitment and thereby produce anti-inflammatory effects and may suppress neutrophil migration through the leukocyte transendothelial migration pathway. TUNEL and RT-PCR experiments revealed that LPS-induced ALI in mice increases the apoptosis of lung tissues, damage to alveolar epithelial cells and levels of inflammatory factors. Treatment with isorhynchophylline can repair tissues, improve lung tissue pathology and reduce lung inflammation.
Project description:The lung is a barrier tissue with constant exposure to the inhaled environment. Therefore, innate immunity against particulates and pathogens is of critical importance to maintain tissue homeostasis. While the lung harbors both myelinating and non-myelinating Schwann cells (NMSCs), NMSCs represent the abundant Schwann cell (SC) population in the lung. However, their contribution to lung physiology remains largely unknown. Here, we used the human glial fibrillary acidic protein promoter (GFAP) driving tdTomato expression in mice to identify SCs in the peripheral nervous system (PNS) and determine their location within the lung. Single-cell transcriptomic analysis revealed the existence of two NMSC populations (NMSC1 and NMSC2) that may participate in pathogen recognition. We demonstrated that these pulmonary SCs produce chemokines and cytokines upon lipopolysaccharide (LPS) stimulation using in vitro conditions. Furthermore, we challenged mouse lungs with LPS and found that NMSC1 exhibits an enriched pro-inflammatory response among all SC subtypes. Collectively, these findings define the molecular profiles of lung SCs and suggest a potential role for NMSCs in lung inflammation.
Project description:The lung is a barrier tissue with constant exposure to the inhaled environment. Therefore, innate immunity against particulates and pathogens is of critical importance to maintain tissue homeostasis. While the lung harbors both myelinating and non-myelinating Schwann cells (NMSCs), NMSCs represent the abundant Schwann cell (SC) population in the lung. However, their contribution to lung physiology remains largely unknown. Here, we used the human glial fibrillary acidic protein promoter (GFAP) driving tdTomato expression in mice to identify SCs in the peripheral nervous system (PNS) and determine their location within the lung. Single-cell transcriptomic analysis revealed the existence of two NMSC populations (NMSC1 and NMSC2) that may participate in pathogen recognition. We demonstrated that these pulmonary SCs produce chemokines and cytokines upon lipopolysaccharide (LPS) stimulation using in vitro conditions. Furthermore, we challenged mouse lungs with LPS and found that NMSC1 exhibits an enriched pro-inflammatory response among all SC subtypes. Collectively, these findings define the molecular profiles of lung SCs and suggest a potential role for NMSCs in lung inflammation.
Project description:We developed a two-staged lung cancer mouse model, which mimics the smoking carcinogen-induced, and chronic obstructive pulmonary disease (COPD)-related airway inflammation promoted lung cancers. We used the carcinogen 4-(methylnitrosamino)-1-(3- pyridyl)-1-butanone (NNK) to induce lung cancer and in parallel to repeated Lipopolysaccharide (LPS) installation to induce chronic lung inflammation. To identify genes associated with chronic inflammation promoting lung tumorigenesis, we have performed whole genome microarray expression profiling of mice exposed to Phosphate-Buffered Saline (PBS), NNK, LPS, and combined NNK and LPS.