Digital gene expression analysis of transcriptomes in lipopolysaccharide-induced acute respiratory distress syndrome

Lv, Xue; Zhang, Yong juan; Lü, Wei; Wang, Qin; Li, Shao ying; Guo, Liang; Gui, Qian; Zhou, Simin; Li, Yu ying

doi:10.1016/j.cca.2015.07.018

Cited by 4 publications

(5 citation statements)

References 46 publications

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“…Several reports have demonstrated that CXCL1, CXCL2, and JE (the murine homolog of human CCL2) accumulated in bronchoalveolar lavage fluid from mice with HCl- or LPS-induced ARDS, CCL2 in bleomycin-injured mouse lungs, CXCL2 and 9 in LPS-treated mouse serum and lung, and mRNA expression of CCL2 in lungs from repeated saline lavage-induced and mechanical ventilation-induced rats, CCL2 and 7 in bronchoalveolar lavage fluid from LPS-challenged volunteers and ARDS patients, and the mRNA and protein expression of CCL2 in LPS-treated RAW264.7 cells [ 31 , 47 – 53 ]. As mentioned in a recent study, CCL2 and 7 and CXCL1, 10, and 11 showed significantly different expression levels in lung tissues from LPS-induced ARDS mice by digital gene expression analysis [ 54 ]. In a previous study, the production of CCL2 was blocked and thereby decreased the influx of inflammatory cells during lung injury [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Candidate Genes as Biomarkers in Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome Based on mRNA Expression Profile by Next-Generation RNA-Seq Analysis

Wan

2018

BioMed Research International

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Up until now, the regulation mechanism at the level of gene during lipopolysaccharide- (LPS-) induced acute respiratory distress syndrome (ARDS) remains unclear. The discovery of differentially expressed genes (DEGs) between LPS-induced ARDS rats and normal rats by next-generation RNA sequencing analysis is of particular interest for the current study. These DEGs may help clinical diagnosis of ARDS and facilitate the selection of the optimal treatment strategy. Randomly, 20 rats were equally divided into 2 groups, the control group and the LPS group. Three rats from each group were selected at random for RNA sequencing analysis. Sequence reads were obtained from Illumina HiSeq4000 and mapped onto the rat reference genome RN6 using Hisat2. We identified 5244 DEGs (Fold_Change > 1.5, and P < 0.05) in the lung tissues from LPS-treated rats compared with normal rats, including 1413 upregulated and 3831 downregulated expressed genes. Lots of chemokine family members were among the most upregulated genes in LPS group. Gene ontology (GO) analysis revealed that almost all of the most enriched and meaningful biological process terms were mainly involved in the functions like immune-inflammation response and the pathways like cytokine-cytokine receptor interaction. We also found that, as for GO molecular function terms, the enriched terms were mainly related to chemokines and cytokines. DEGs with fold change over 100 were verified by quantitative real-time polymerase chain reaction and reanalyzed by gene-gene coexpression network, and the results elucidated central roles of chemokines in LPS-induced ARDS. Our results revealed some new biomarkers for uncovering mechanisms and processes of ARDS.

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Section: Discussionmentioning

confidence: 99%

Candidate Genes as Biomarkers in Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome Based on mRNA Expression Profile by Next-Generation RNA-Seq Analysis

Wan

2018

BioMed Research International

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“…Microbial proliferation and sepsis following acute lung injury is a primary contributor to the cascade and severity of NRDS. Lv et al ( 32 ) demonstrated through transcriptomic analysis that genes associated with foreign pathogens (NLR family pyrin domain containing 3 and S100 calcium binding protein A8/A9) were markedly upregulated in response to microbial LPS.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to sepsis, other factors not involved with the innate immune response or surfactants may contribute to NRDS and ARDS. For example, Lv et al ( 32 ) demonstrated, through systematic mRNA-seq of ARDS, a significant upregulation of 122 genes and a downregulation of 91 genes associated with essential protein functions, including the mitotic cell cycle. Specifically, the investigators noted that cyclin (CCNB)1 and CCNB2, which serve a role in cell cycle regulation, may be associated with the onset of ARDS.…”

Section: Discussionmentioning

confidence: 99%

Messenger RNA sequencing reveals similar mechanisms between neonatal and acute respiratory distress syndrome

et al. 2017

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Hypoxemia and hypercarbia resulting from a lack of surfactant is considered to be the primary mechanism underlying neonatal respiratory distress syndrome (NRDS). Surfactant replacement therapy may mitigate the symptoms of the disease by decreasing the surface tension of alveoli and facilitating inflation. However, surfactant serves an additional role in immunological processes. Therefore, it may be hypothesized that mechanisms of NRDS involving surfactant exert additional functions to promoting alveolar inflation. Using peripheral blood obtained from mature infants with and without NRDS, in tandem with mRNA sequencing (mRNA-seq) analysis, the present study identified that, while cell cycle regulation and alveolar surfactants serve a role in deterring the further onset of NRDS, innate and pathogen-induced responses of the immune system are among the most important factors in the pathology. The present study illustrated the regulatory importance of these immune pathways in response to alterations in the expression of gene families, particularly in perpetual lung injury leading to NRDS. Notably, data collected from the mRNA-seq analysis revealed similar mechanisms between NRDS and acute respiratory distress syndrome, a clinical phenotype precipitated by the manifestation of a severe form of lung injury due to numerous lung insults, implying that similar therapies may be applied to treat these two diseases.

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“…Most studies to date correspond to animal models, however there are few transcriptomic analyses in ARDS patients. 347 , 456 , 457 …”

Section: Emerging Techniques In Lung Injurymentioning

confidence: 99%

Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques

Keskinidou¹,

Vassiliou²,

Dimopoulou³

et al. 2022

JIR

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Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury characterized by an acute inflammatory response in the lung parenchyma. Hence, it is considered as the most appropriate clinical syndrome to study pathogenic mechanisms of lung inflammation. ARDS is associated with increased morbidity and mortality in the intensive care unit (ICU), while no effective pharmacological treatment exists. It is very important therefore to fully characterize the underlying pathobiology and the related mechanisms, in order to develop novel therapeutic approaches. In vivo and in vitro models are important pre-clinical tools in biological and medical research in the mechanistic and pathological understanding of the majority of diseases. In this review, we will present data from selected experimental models of lung injury/acute lung inflammation, which have been based on clinical disorders that can lead to the development of ARDS and related inflammatory lung processes in humans, including ventilation-induced lung injury (VILI), sepsis, ischemia/reperfusion, smoke, acid aspiration, radiation, transfusion-related acute lung injury (TRALI), influenza, Streptococcus ( S .) pneumoniae and coronaviruses infection. Data from the corresponding clinical conditions will also be presented. The mechanisms related to lung inflammation that will be covered are oxidative stress, neutrophil extracellular traps, mitogen-activated protein kinase (MAPK) pathways, surfactant, and water and ion channels. Finally, we will present a brief overview of emerging techniques in the field of omics research that have been applied to ARDS research, encompassing genomics, transcriptomics, proteomics, and metabolomics, which may recognize factors to help stratify ICU patients at risk, predict their prognosis, and possibly, serve as more specific therapeutic targets.

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Digital gene expression analysis of transcriptomes in lipopolysaccharide-induced acute respiratory distress syndrome

Cited by 4 publications

References 46 publications

Candidate Genes as Biomarkers in Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome Based on mRNA Expression Profile by Next-Generation RNA-Seq Analysis

Candidate Genes as Biomarkers in Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome Based on mRNA Expression Profile by Next-Generation RNA-Seq Analysis

Messenger RNA sequencing reveals similar mechanisms between neonatal and acute respiratory distress syndrome

Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques

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