ArticleMolecular biology reports2012
Kinetic and distinct distribution of conventional dendritic cells in the early phase of lipopolysaccharide-induced acute lung injury.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Modulation of Human Dendritic Cell Functions by Phosphodiesterase-4 Inhibitors: Potential Relevance for the Treatment of Respiratory Diseases.Pharmaceutics · 2023Review
- Role of Cholinergic Anti-Inflammatory Pathway in Protecting Sepsis-Induced Acute Lung Injury through Regulation of the Conventional Dendritic Cells.Mediators of inflammation · 2022Article
- Bone marrow mesenchymal stem cells attenuate LPS-induced acute lung injury in mice by promoting RvE1/ProD1 and modulating Treg/Th17 balance.Turkish journal of biology = Turk biyoloji dergisi · 2022Article
- Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells' maturation and function.Open life sciences · 2021Article
- Apolipoprotein M Protects Against Lipopolysaccharide-Induced Acute Lung Injury via Sphingosine-1-Phosphate Signaling.Inflammation · 2018Article
- Blockage of thymic stromal lymphopoietin signaling improves acute lung injury in mice by regulating pulmonary dendritic cells.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Respiratory dendritic cells (DCs), especially conventional DCs (cDCs), are critically involved in the induction phase of the immune response in the respiratory system. However, little information concerning cDC kinetics in acute lung injury (ALI) is available. In this study, we have used a murine model of LPS-induced ALI to examine the kinetics and phenotype of respiratory, circulating and splenic cDCs. cDCs in the lung, blood, and spleen and the IL-6 level in the lung were detected at 6, 12 and 24 h after PBS or LPS challenge. In the ALI group, a rapid cDCs accumulation in the lung was observed, and there were highly significant correlations between the frequency of respiratory cDCs or the percentage of cDC expressing CD80 and the IL-6 concentration. However, the frequency of peripheral blood cDCs decreased rapidly in ALI mice, followed by a marked expansion. In addition, splenic cDCs only showed a transient expansion in ALI. cDCs within the blood, lungs and spleens had undergone a modest maturation in the ALI group. Our findings demonstrate that LPS-induced ALI provokes a dynamic and distinct distribution as well as phenotype changes in pulmonary, circulatory and splenic cDC populations. Lung cDCs may participate in the early inflammatory response to ALI.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.