ArticleJournal of innate immunity2013
Staphylococcus aureus proteases degrade lung surfactant protein A potentially impairing innate immunity of the lung.
Article in Journal of innate immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- The endothelium at the interface between tissues andClinical microbiology reviews · 2025Review
- Exploring Proteases as Alternative Molecular Targets to Tackle Inflammation in Cystic Fibrosis Respiratory Infections.International journal of molecular sciences · 2025Review
- The major role ofVirulence · 2023Article
- Identification and classification of papain-like cysteine proteinases.The Journal of biological chemistry · 2023Article
- The collectin SP-A and its trimeric recombinant fragment protect alveolar epithelial cells from the cytotoxic and proinflammatory effects of human cathelicidinFrontiers in immunology · 2022Article
- Skin-to-blood pH shift triggers metabolome and proteome global remodelling inFrontiers in microbiology · 2022Article
- Intracellular Staphylococcus aureus employs the cysteine protease staphopain A to induce host cell death in epithelial cells.PLoS pathogens · 2021Article
- Review
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- Antimicrobial Peptide Induced-Stress RendersFrontiers in immunology · 2020Article
- Review
- Advanced Role of Neutrophils in Common Respiratory Diseases.Journal of immunology research · 2017Review
- Extracellular Bacterial Proteases in Chronic Wounds: A Potential Therapeutic Target?Advances in wound care · 2016Review
- Fluid phase recognition molecules in neutrophil-dependent immune responses.Seminars in immunology · 2016Review
- Serum Lipoproteins Are Critical for Pulmonary Innate Defense against Staphylococcus aureus Quorum Sensing.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Identification of Secreted Exoproteome Fingerprints of Highly-Virulent and Non-Virulent Staphylococcus aureus Strains.Frontiers in cellular and infection microbiology · 2016Article
- Article
- All that glisters is not gold - Staphylococcus aureus and innate immunity.Journal of innate immunity · 2015Article
- Impact of the functional status of saeRS on in vivo phenotypes of Staphylococcus aureus sarA mutants.Molecular microbiology · 2014Article
- Surveillance and countermeasures in innate immunity.Journal of innate immunity · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The pulmonary surfactant is a complex mixture of lipids and proteins that is important for respiratory lung functions, which also provides the first line of innate immune defense. Pulmonary surfactant protein-A (SP-A) is a major surfactant component with immune functions with importance during Staphylococcus aureus infections that has been demonstrated in numerous studies. The current study showed that S. aureus can efficiently cleave the SP-A protein using its arsenal of proteolytic enzymes. This degradation appears to be mediated by cysteine proteases, in particular staphopain A (ScpA). The staphopain-mediated proteolysis of SP-A resulted in a decrease or complete abolishment of SP-A biological activity, including the promotion of S. aureus phagocytosis by neutrophils, aggregation of Gram-negative bacteria and bacterial cell adherence to epithelium. Significantly, ScpA has also efficiently degraded SP-A in complete bronchi-alveolar lavage fluid from human lungs. This indicates that staphopain activity in the lungs is resistant to protease inhibitors, thus suggesting that SP-A can be cleaved in vivo. Collectively, this study showed that the S. aureus protease ScpA is an important virulence factor that may impair innate immunity of the lungs.
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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.