ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Respiratory syncytial virus infection alters surfactant protein A expression in human pulmonary epithelial cells by reducing translation efficiency.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Multiomics as instrument to promote 3P medical approaches for the overall management of respiratory syncytial viral infections.The EPMA journal · 2025Review
- Dynamic Fluid Flow Exacerbates the (Pro-)Inflammatory Effects of Aerosolised Engineered Nanomaterials In Vitro.Nanomaterials (Basel, Switzerland) · 2022Article
- Maternal and neonatal risk factors for neonatal respiratory distress syndrome in term neonates in Cyprus: a prospective case-control study.Italian journal of pediatrics · 2021Article
- A primate-specific RNA-binding protein (RBMXL3) is involved in glucocorticoid regulation of human pulmonary surfactant protein B (SP-B) mRNA stability.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Review
- Identification of the interferon-inducible GTPase GBP1 as major restriction factor for the Hepatitis E virus.Journal of virology · 2021Article
- Infections of the lung: a predictive, preventive and personalized perspective through the lens of evolution, the emergence of SARS-CoV-2 and its pathogenesis.The EPMA journal · 2020Review
- Innate Immune Evasion by Human Respiratory RNA Viruses.Journal of innate immunity · 2020Review
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Sensitization of avian pathogenic Escherichia coli to amoxicillin in vitro and in vivo in the presence of surfactin.PloS one · 2019Article
- Viral-Bacterial Co-infections in the Cystic Fibrosis Respiratory Tract.Frontiers in immunology · 2018Review
- The Role of Surfactant in Lung Disease and Host Defense against Pulmonary Infections.Annals of the American Thoracic Society · 2015Review
- An 11-nt sequence polymorphism at the 3'UTR of human SFTPA1 and SFTPA2 gene variants differentially affect gene expression levels and miRNA regulation in cell culture.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Review
- Article
- Exon B of human surfactant protein A2 mRNA, alone or within its surrounding sequences, interacts with 14-3-3; role of cis-elements and secondary structure.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- An Insight into the Diverse Roles of Surfactant Proteins, SP-A and SP-D in Innate and Adaptive Immunity.Frontiers in immunology · 2012Article
- Air pollution and epigenetics: effects on SP-A and innate host defence in the lung.Swiss medical weekly · 2012Review
- Infant formula alters surfactant protein A (SP-A) and SP-B expression in pulmonary epithelial cells.Pediatric pulmonology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Infection of neonatal lung by respiratory syncytial virus (RSV) is a common cause of respiratory dysfunction. Lung alveolar type II and bronchiolar epithelial (Clara) cells secrete surfactant protein A (SP-A), a collectin that is an important component of the pulmonary innate immune system. SP-A binds to the virus, targeting the infectious agent for clearance by host defense mechanisms. We have previously shown that while the steady-state level of SP-A mRNA increases approximately threefold after RSV infection, steady-state levels of cellular and secreted SP-A protein decrease 40-60% in human type II cells in primary culture, suggesting a mechanism where the virus alters components of the innate immune response in infected cells. In these studies, we find that changes in SP-A mRNA and protein levels in RSV-infected NCI-H441 cells (a bronchiolar epithelial cell line) recapitulate the results in SP-A expression observed in primary lung cells. While SP-A protein is normally ubiquitinated, there is no change in the level of SP-A protein ubiquitination or proteasome activity during RSV infection, suggesting that the reduced levels of SP-A protein are not due to degradation by activated proteasomes. SP-A mRNA is appropriately processed and exported from the nucleus to the cytoplasm during RSV infection. As evidenced by polysome analysis of SP-A mRNA and pulse-chase analysis of newly synthesized SP-A protein, we find a decrease in translational efficiency that is specific for SP-A mRNA. Therefore, the decrease in SP-A protein levels observed after RSV infection of pulmonary bronchiolar epithelial cells results from a mechanism that affects SP-A mRNA translation efficiency.
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Registered trials
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