ArticleClinical and experimental immunology2008
The mechanism of development of acute lung injury in lethal endotoxic shock using alpha-galactosylceramide sensitization.
Article in Clinical and experimental immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 33 citations in OpenAlex.
- Pyroptosis of pulmonary fibroblasts and macrophages through NLRC4 inflammasome leads to acute respiratory failure.Cell reports · 2025Article
- Aggravated intestinal ischemia‑reperfusion injury is associated with activated mitochondrial autophagy in a mouse model of diabetes.Molecular medicine reports · 2020Article
- An Active Drimane-Type Lactone from Polygonum jucundum Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Mice Through TLR4-MAPKs Signaling Pathway.Inflammation · 2017Article
- CD1d- and MR1-Restricted T Cells in Sepsis.Frontiers in immunology · 2015Review
- Anti-inflammatory effects of Reduning Injection on lipopolysaccharide-induced acute lung injury of rats.Chinese journal of integrative medicine · 2014Article
- Modulation of LPS-stimulated pulmonary inflammation by Borneol in murine acute lung injury model.Inflammation · 2014Article
- Anti-inflammatory effect of selagin-7-O-(6''-O-acetyl-)-ß-D-glycoside isolated from Cancrinia discoidea on lipopolysaccharide-induced mouse macrophage RAW 264.7 cells.EXCLI journal · 2014Article
- A critical role for Lyn kinase in strengthening endothelial integrity and barrier function.Blood · 2013Article
- The melanocortin 1 receptor (MC1R) inhibits the inflammatory response in Raw 264.7 cells and atopic dermatitis (AD) mouse model.Molecular biology reports · 2013Article
- Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- CD1d-independent activation of invariant natural killer T cells by staphylococcal enterotoxin B through major histocompatibility complex class II/T cell receptor interaction results in acute lung injury.Infection and immunity · 2011Article
- Endotoxin-induced lung injury in α-galactosylceramide-sensitized mice is caused by failure of interleukin-4 production in lung natural killer T cells.Clinical and experimental immunology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism underlying acute lung injury in lethal endotoxic shock induced by administration of lipopolysaccharide (LPS) into alpha-galactosylceramide (alpha-GalCer)-sensitized mice was studied. Sensitization with alpha-GalCer resulted in the increase of natural killer T (NK T) cells and the production of interferon (IFN)-gamma in the lung. The IFN-gamma that was produced induced expression of adhesion molecules, especially vascular cell adhesion molecule-1 (VCAM-1), on vascular endothelial cells in the lung. Anti-IFN-gamma antibody inhibited significantly the VCAM-1 expression in alpha-GalCer-sensitized mice. Very late activating antigen-4-positive cells, as the counterpart of VCAM-1, accumulated in the lung. Anti-VCAM-1 antibody prevented LPS-mediated lethal shock in alpha-GalCer-sensitized mice. The administration of LPS into alpha-GalCer-sensitized mice caused local production of excessive proinflammatory mediators, such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6 and nitric oxide. LPS caused microvascular leakage of proteins and cells into bronchoalveolar lavage fluid. Taken together, sensitization with alpha-GalCer was suggested to induce the expression of VCAM-1 via IFN-gamma produced by NK T cells and recruit a number of inflammatory cells into the lung. Further, LPS was suggested to lead to the production of excessive proinflammatory mediators, the elevation of pulmonary permeability and cell death. The putative mechanism of acute lung injury in LPS-mediated lethal shock using alpha-GalCer sensitization is discussed.
Indexed as
Identifiers
What OpenQuestion holds
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.