ArticleAmerican journal of respiratory cell and molecular biology2013
Persistence of LPS-induced lung inflammation in surfactant protein-C-deficient mice.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- Recombinant human mitsugumin 53: a potential therapeutic agent for multiple diseases.Frontiers in pharmacology · 2025Review
- Bacterial expression, purification and folding of exceptionally hydrophobic and essential protein: Surfactant Protein-B (SP-B).PloS one · 2025Article
- Hippo cooperates with p53 to regulate lung airway mucous cell metaplasia.Disease models & mechanisms · 2024Article
- Review
- LncRNA HOTTIP promotes LPS-induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP-C.Journal of cell communication and signaling · 2024Article
- Role of DCLK1/Hippo pathway in type II alveolar epithelial cells differentiation in acute respiratory distress syndrome.Molecular medicine (Cambridge, Mass.) · 2023Article
- Regulation of Surfactant Protein Gene Expression byMicroorganisms · 2023Article
- IGF1R as a Potential Pharmacological Target in Allergic Asthma.Biomedicines · 2021Article
- Role and mechanisms of autophagy in lung metabolism and repair.Cellular and molecular life sciences : CMLS · 2021Review
- Regulation of Immune Responses by Nonhematopoietic Cells in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Bone marrow-derived mesenchymal stem cells attenuate pulmonary inflammation and lung damage caused by highly pathogenic avian influenza A/H5N1 virus in BALB/c mice.BMC infectious diseases · 2020Article
- TRIM72 promotes alveolar epithelial cell membrane repair and ameliorates lung fibrosis.Respiratory research · 2020Article
- Lipid-Protein and Protein-Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis.International journal of molecular sciences · 2020Review
- Crystal Deposits in Macrophages and Distal Lung Remodeling: A Tale of Aging in SFTPC-Deficient Mice.American journal of respiratory cell and molecular biology · 2020Article
- Aging and Lung Disease.Annual review of physiology · 2020Review
- Alveolar Dynamics and Beyond - The Importance of Surfactant Protein C and Cholesterol in Lung Homeostasis and Fibrosis.Frontiers in physiology · 2020Review
- Organic dust inhibits surfactant protein expression by reducing thyroid transcription factor-1 levels in human lung epithelial cells.Innate immunity · 2019Article
- Mediastinal lymphadenopathy reflecting disease activity in an infant with chronic pneumonitis of infancy associated with surfactant protein C mutation: a case report and literature review.Journal of thoracic disease · 2018Article
- Surfactant protein C dampens inflammation by decreasing JAK/STAT activation during lung repair.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Site-specific and endothelial-mediated dysfunction of the alveolar-capillary barrier in response to lipopolysaccharides.Journal of cellular and molecular medicine · 2018Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Pulmonary surfactant protein-C (SP-C) gene-targeted mice (Sftpc(-/-)) develop progressive lung inflammation and remodeling. We hypothesized that SP-C deficiency reduces the ability to suppress repetitive inflammatory injury. Sftpc(+/+) and Sftpc(-/-) mice given three doses of bacterial LPS developed airway and airspace inflammation, which was more intense in the Sftpc(-/-) mice at 3 and 5 days after the final dose. Compared with Sftpc(+/+)mice, inflammatory injury persisted in the lungs of Sftpc(-/-) mice 30 days after the final LPS challenge. Sftpc(-/-) mice showed LPS-induced airway goblet cell hyperplasia with increased detection of Sam pointed Ets domain and FoxA3 transcription factors. Sftpc(-/-) type II alveolar epithelial cells had increased cytokine expression after LPS exposure relative to Sftpc(+/+) cells, indicating that type II cell dysfunction contributes to inflammatory sensitivity. Microarray analyses of isolated type II cells identified a pattern of enhanced expression of inflammatory genes consistent with an intrinsic low-level inflammation resulting from SP-C deficiency. SP-C-containing clinical surfactant extract (Survanta) or SP-C/phospholipid vesicles blocked LPS signaling through the LPS receptor (Toll-like receptor [TLR] 4/CD14/MD2) in human embryonic kidney 293T cells, indicating that SP-C blocks LPS-induced cytokine production by a TLR4-dependent mechanism. Phospholipid vesicles alone did not modify the TLR4 response. In vivo deficiency of SP-C leads to inflammation, increased cytokine production by type II cells, and persistent inflammation after repetitive LPS stimulation.
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