ArticleAmerican journal of respiratory cell and molecular biology2011
Fas activation in alveolar epithelial cells induces KC (CXCL1) release by a MyD88-dependent mechanism.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Phagocytosis is a primary determinant of pulmonary clearance of clinicalFrontiers in cellular and infection microbiology · 2023Article
- The bioactivity of soluble Fas ligand is modulated by key amino acids of its stalk region.PloS one · 2021Article
- Article
- Effects of Keratinocyte-Derived Cytokine (CXCL-1) on the Development of Theiler's Virus-Induced Demyelinating Disease.Frontiers in cellular and infection microbiology · 2018Article
- Cytokine-Ion Channel Interactions in Pulmonary Inflammation.Frontiers in immunology · 2017Review
- HMGB1 release triggered by the interaction of live retinal cells and uveitogenic T cells is Fas/FasL activation-dependent.Journal of neuroinflammation · 2015Article
- p120-catenin expressed in alveolar type II cells is essential for the regulation of lung innate immune response.The American journal of pathology · 2015Article
- Disruption of fas-fas ligand signaling, apoptosis, and innate immunity by bacterial pathogens.PLoS pathogens · 2014Review
- The peripheral whole-blood transcriptome of acute pyelonephritis in human pregnancya.Journal of perinatal medicine · 2014Article
- Myeloperoxidase deficiency in mice exacerbates lung inflammation induced by nonviable Candida albicans.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
- Life in the Fas lane: differential outcomes of Fas signaling.Cellular and molecular life sciences : CMLS · 2013Review
- The Fas/FasL pathway impairs the alveolar fluid clearance in mouse lungs.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Fas-deficient mice have impaired alveolar neutrophil recruitment and decreased expression of anti-KC autoantibody:KC complexes in a model of acute lung injury.Respiratory research · 2012Article
- Role of the Fas/FasL system in a model of RSV infection in mechanically ventilated mice.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Death receptors mediate the adverse effects of febrile-range hyperthermia on the outcome of lipopolysaccharide-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2011Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Activation of the Fas/Fas ligand (FasL) system is associated with activation of apoptotic and proinflammatory pathways that lead to the development of acute lung injury. Previous studies in chimeric mice and macrophage-depleted mice suggested that the main effector cell in Fas-mediated lung injury is not a myeloid cell, but likely an epithelial cell. The goal of this study was to determine whether epithelial cells release proinflammatory cytokines after Fas activation, and to identify the relevant pathways. Incubation of the murine alveolar epithelial cell line, MLE-12, with the Fas-activating monoclonal antibody, Jo2, resulted in release of the CXC chemokine, KC, in a dose-dependent manner. KC release was not prevented by the pan-caspase inhibitor, zVAD.fmk. Silencing of the adaptor protein, MyD88, with small interfering (si)RNA resulted in attenuation of KC release in response to Jo2. Fas activation resulted in phosphorylation of the mitogen-activated kinases extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK), and pharmacologic inhibition of ERK and JNK attenuated KC release in a dose-response manner. Similarly, primary human small airways epithelial cells released IL-8 in response to soluble FasL, and this was abrogated by inhibition of JNK and ERK. In vivo confirmatory studies showed that MyD88-null mice are protected from Fas-induced acute lung injury. In summary, we conclude that Fas induces KC release in MLE-12 cells by a mechanism requiring MyD88, mitogen-activated protein kinases, and likely activator protein-1.
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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.