ArticleRespiratory research2013
Genetic replacement of surfactant protein-C reduces respiratory syncytial virus induced lung injury.
Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 41 citations in OpenAlex.
- Metabolic Reprogramming-Related Genes in Lung Adenocarcinoma: Identification and Prognostic Model Construction.World journal of oncology · 2025Article
- Surfactant Protein-C Regulates Alveolar Type 2 Epithelial Cell Lineages via the CD74 Receptor.Journal of respiratory biology and translational medicine · 2024Article
- LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C.Journal of cell communication and signaling · 2024Article
- Towards personalized therapies for genetic disorders of surfactant dysfunction.Seminars in fetal & neonatal medicine · 2023Review
- Article
- Alveolar Dynamics and Beyond - The Importance of Surfactant Protein C and Cholesterol in Lung Homeostasis and Fibrosis.Frontiers in physiology · 2020Review
- Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Recurrent diffuse lung disease due to surfactant protein C deficiency.Respiratory medicine case reports · 2018Article
- Regulation of p53-mediated changes in the uPA-fibrinolytic system and in lung injury by loss of surfactant protein C expression in alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- HMGB1 induces lung fibroblast to myofibroblast differentiation through NF‑κB‑mediated TGF‑β1 release.Molecular medicine reports · 2017Article
- Surfactant Protein C-associated interstitial lung disease; three different phenotypes of the same SFTPC mutation.Italian journal of pediatrics · 2016Article
- Host genes and influenza pathogenesis in humans: an emerging paradigm.Current opinion in virology · 2015Review
- Surfactant dysfunction and lung inflammation in the female mouse model of lymphangioleiomyomatosis.American journal of respiratory cell and molecular biology · 2015Article
- Diseases of pulmonary surfactant homeostasis.Annual review of pathology · 2015Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundIndividuals with deficiencies of pulmonary surfactant protein C (SP-C) develop interstitial lung disease (ILD) that is exacerbated by viral infections including respiratory syncytial virus (RSV). SP-C gene targeted mice (Sftpc -/-) lack SP-C, develop an ILD-like disease and are susceptible to infection with RSV.
methodsIn order to determine requirements for correction of RSV induced injury we have generated compound transgenic mice where SP-C expression can be induced on the Sftpc -/- background (SP-C/Sftpc -/-) by the administration of doxycycline (dox). The pattern of induced SP-C expression was determined by immunohistochemistry and processing by Western blot analysis. Tissue and cellular inflammation was measured following RSV infection and the RSV-induced cytokine response of isolated Sftpc +/+ and -/- type II cells determined.
resultsAfter 5 days of dox administration transgene SP-C mRNA expression was detected by RT-PCR in the lungs of two independent lines of bitransgenic SP-C/Sftpc -/- mice (lines 55.3 and 54.2). ProSP-C was expressed in the lung, and mature SP-C was detected by Western blot analysis of the lavage fluid from both lines of SP-C/Sftpc -/- mice. Induced SP-C expression was localized to alveolar type II cells by immunostaining with an antibody to proSP-C. Line 55.3 SP-C/Sftpc -/- mice were maintained on or off dox for 7 days and infected with 2.6x107 RSV pfu. On day 3 post RSV infection total inflammatory cell counts were reduced in the lavage of dox treated 55.3 SP-C/Sftpc -/- mice (p = 0.004). The percentage of neutrophils was reduced (p = 0.05). The viral titers of lung homogenates from dox treated 55.3 SP-C/Sftpc -/- mice were decreased relative to 55.3 SP-C/Sftpc -/- mice without dox (p = 0.01). The cytokine response of Sftpc -/- type II cells to RSV was increased over that of Sftpc +/+ cells.
conclusionsTransgenic restoration of SP-C reduced inflammation and improved viral clearance in the lungs of SP-C deficient mice. The loss of SP-C in alveolar type II cells compromises their response to infection. These findings show that the restoration of SP-C in Sftpc -/- mice in response to RSV infection is a useful model to determine parameters for therapeutic intervention.
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