ArticleAmerican journal of respiratory cell and molecular biology2012
Virus-infected alveolar epithelial cells direct neutrophil chemotaxis and inhibit their apoptosis.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- The Role of Alpha-1 Antitrypsin in the Pathophysiology and Treatment of Inflammatory Lung Diseases.Journal of inflammation research · 2026Review
- Chemokine Cxcl1-Cxcl2 heterodimer is a potent neutrophil chemoattractant.Journal of leukocyte biology · 2023Article
- Neutrophils at the crossroads of acute viral infections and severity.Molecular aspects of medicine · 2021Review
- Computational and Transcriptome Analyses Revealed Preferential Induction of Chemotaxis and Lipid Synthesis by SARS-CoV-2.Biology · 2020Article
- Respiratory epithelial cells as master communicators during viral infections.Current clinical microbiology reports · 2019Article
- Chemokine CXCL7 Heterodimers: Structural Insights, CXCR2 Receptor Function, and Glycosaminoglycan Interactions.International journal of molecular sciences · 2017Article
- Lung epithelial cells have virus-specific and shared gene expression responses to infection by diverse respiratory viruses.PloS one · 2017Article
- Effects and mechanisms of alveolar type II epithelial cell apoptosis in severe pancreatitis-induced acute lung injury.Experimental and therapeutic medicine · 2014Article
- Neutrophils are needed for an effective immune response against pulmonary rat coronavirus infection, but also contribute to pathology.The Journal of general virology · 2014Article
- Differentiated phenotypes of primary murine alveolar epithelial cells and their susceptibility to infection by respiratory viruses.Virus research · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The alveolar epithelium is a critical target for pulmonary viruses and can produce proinflammatory cytokines and chemokines upon viral infection. However, the molecular interactions between virus-infected alveolar epithelial cells and inflammatory cells, including polymorphonuclear leukocytes (PMNs), have not been thoroughly characterized. Rat coronavirus (RCoV) is used as a model to study the immune response to viral infection in the lung of the natural host. We have developed an in vitro model to characterize the response of PMNs to RCoV-infected type I-like alveolar epithelial (AT1) cells, the primary target for RCoV infection in the alveoli. Multiple CXC chemokines that signal through CXCR2 were required for PMN chemotaxis toward medium from RCoV-infected AT1-like cells (RCoV-AT1). Furthermore, RCoV-AT1 inhibited spontaneous PMN apoptosis, including activation of effector caspase 3 and initiator caspases 8 and 9. Use of a selective inhibitor of CXCR2, SB265610, demonstrated that CXCR2 signaling was required for RCoV-AT1-mediated inhibition of PMN apoptosis. These data suggest that CXC chemokines produced by RCoV-infected AT1-like cells inhibit PMN apoptosis during infection. These studies provide new insight into the molecular mechanisms whereby alveolar epithelial cells direct the functions of PMNs during viral infection of the lung.
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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.