ArticlePloS one2012
Surfactant protein-A suppresses eosinophil-mediated killing of Mycoplasma pneumoniae in allergic lungs.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 38 citations in OpenAlex.
- The virome composition of respiratory tract changes in school-aged children with Mycoplasma pneumoniae infection.Virology journal · 2025Article
- The Immune Modulatory Role of Surfactants inJournal of inflammation research · 2025Review
- Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024Review
- SURFACTANT PROTEIN A: AN INNATE IMMUNE MODULATOR AND THERAPEUTIC IN ASTHMA.Transactions of the American Clinical and Climatological Association · 2024Review
- Creatine Kinase Is Decreased in Childhood Asthma.American journal of respiratory and critical care medicine · 2023Article
- Interaction between alveolar macrophages and epithelial cells duringFrontiers in cellular and infection microbiology · 2023Review
- Impact of Therapeutics on Unified Immunity During Allergic Asthma and Respiratory Infections.Frontiers in allergy · 2022Review
- Small Peptide Derivatives Within the Carbohydrate Recognition Domain of SP-A2 Modulate Asthma Outcomes in Mouse Models and Human Cells.Frontiers in immunology · 2022Article
- Myeloid-associated differentiation marker is a novel SP-A-associated transmembrane protein whose expression on airway epithelial cells correlates with asthma severity.Scientific reports · 2021Article
- IGF1R as a Potential Pharmacological Target in Allergic Asthma.Biomedicines · 2021Article
- Prevalence and clinical characteristics of septicemia in children withThe Journal of international medical research · 2021Article
- miR-143-3p impacts on pulmonary inflammatory factors and cell apoptosis in mice with mycoplasmal pneumonia by regulating TLR4/MyD88/NF-κB pathway.Bioscience reports · 2020Article
- Surfactant Protein-A Protects against IL-13-Induced Inflammation in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Genetic Variation in Surfactant Protein-A2 Delays Resolution of Eosinophilia in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Preformulation and Evaluation of Tofacitinib as a Therapeutic Treatment for Asthma.AAPS PharmSciTech · 2019Article
- Club Cell Secretory Protein Deficiency Leads to Altered Lung Function.American journal of respiratory and critical care medicine · 2019Article
- Eosinophilic and Noneosinophilic Asthma.American journal of respiratory and critical care medicine · 2018Review
- The Emerging Roles of Surfactant Protein-A in Asthma.Journal of clinical & cellular immunology · 2018Article
- Mycoplasma pneumoniae from the Respiratory Tract and Beyond.Clinical microbiology reviews · 2017Review
- Insights into the pathogenesis of Mycoplasma pneumoniae (Review).Molecular medicine reports · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Surfactant protein-A (SP-A) has well-established functions in reducing bacterial and viral infections but its role in chronic lung diseases such as asthma is unclear. Mycoplasma pneumoniae (Mp) frequently colonizes the airways of chronic asthmatics and is thought to contribute to exacerbations of asthma. Our lab has previously reported that during Mp infection of non-allergic airways, SP-A aides in maintaining airway homeostasis by inhibiting an overzealous TNF-alpha mediated response and, in allergic mice, SP-A regulates eosinophilic infiltration and inflammation of the airway. In the current study, we used an in vivo model with wild type (WT) and SP-A(-/-) allergic mice challenged with the model antigen ovalbumin (Ova) that were concurrently infected with Mp (Ova+Mp) to test the hypothesis that SP-A ameliorates Mp-induced stimulation of eosinophils. Thus, SP-A could protect allergic airways from injury due to release of eosinophil inflammatory products. SP-A deficient mice exhibit significant increases in inflammatory cells, mucus production and lung damage during concurrent allergic airway disease and infection (Ova+Mp) as compared to the WT mice of the same treatment group. In contrast, SP-A deficient mice have significantly decreased Mp burden compared to WT mice. The eosinophil specific factor, eosinophil peroxidase (EPO), which has been implicated in pathogen killing and also in epithelial dysfunction due to oxidative damage of resident lung proteins, is enhanced in samples from allergic/infected SP-A(-/-) mice as compared to WT mice. In vitro experiments using purified eosinophils and human SP-A suggest that SP-A limits the release of EPO from Mp-stimulated eosinophils thereby reducing their killing capacity. These findings are the first to demonstrate that although SP-A interferes with eosinophil-mediated biologic clearance of Mp by mediating the interaction of Mp with eosinophils, SP-A simultaneously benefits the airway by limiting inflammation and damage.
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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.