ArticlePloS one2009
Analysis of pulmonary inflammation and function in the mouse and baboon after exposure to Mycoplasma pneumoniae CARDS toxin.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 94 citations in OpenAlex.
- Host immune dysfunction and Mycoplasma pneumoniae immune evasion: dual drivers of pathogenesis in Mycoplasma pneumoniae pneumonia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
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- Bacterial Toxin Exploits Host Membrane Phospholipid as a Receptor for Binding, Entry, and Cytopathogenicity.Molecular microbiology · 2026Article
- Immune dysregulation inFrontiers in immunology · 2026Review
- Study on Baicalin Treatment ofDrug design, development and therapy · 2026Article
- [Respiratory infection with mucocutaneous lesions : A rare manifestation of a known pathogen].Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2025Article
- Chronic Exposure to Two Regimens of Waterpipe Smoke Elicits Lung Injury, Genotoxicity, and Mitochondrial Impairment with the Involvement of MAPKs Activation in Mice.International journal of molecular sciences · 2025Article
- CCL20 Expression via AKT-ERK1/2-AP1 Pathway inJournal of inflammation research · 2025Article
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- Yinqin Qingfei granules alleviateFrontiers in pharmacology · 2024Article
- Regulatory functional role of NLRP3 inflammasome during Mycoplasma hyopneumoniae infection in swine.Journal of animal science · 2023Article
- Global research trends ofFrontiers in pediatrics · 2023Review
- Categorizing Sequences of Concern by Function To Better Assess Mechanisms of Microbial Pathogenesis.Infection and immunity · 2022Review
- RefractoryJournal of clinical medicine · 2022Review
- Molecular Approaches for the Validation of the Baboon as a Nonhuman Primate Model for the Study of Zika Virus Infection.Frontiers in cellular and infection microbiology · 2022Article
- Neutrophil-Mediated Lung Injury Both via TLR2-Dependent Production of IL-1α and IL-12 p40, and TLR2-Independent CARDS Toxin after Mycoplasma pneumoniae Infection in Mice.Microbiology spectrum · 2021Article
- Secreted MbovP0145 Promotes IL-8 Expression through Its Interactive β-Actin and MAPK Activation and Contributes to Neutrophil Migration.Pathogens (Basel, Switzerland) · 2021Article
- Review
- Mycoplasma pneumoniae CARDS toxin exploits host cell endosomal acidic pH and vacuolar ATPase proton pump to execute its biological activities.Scientific reports · 2021Article
- Comparison of different detection methods for Mycoplasma pneumoniae infection in children with community-acquired pneumonia.BMC pediatrics · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Mycoplasma pneumoniae produces an ADP-ribosylating and vacuolating toxin known as the CARDS (Community Acquired Respiratory Distress Syndrome) toxin that has been shown to be cytotoxic to mammalian cells in tissue and organ culture. In this study we tested the ability of recombinant CARDS (rCARDS) toxin to elicit changes within the pulmonary compartment in both mice and baboons. Animals responded to a respiratory exposure to rCARDS toxin in a dose and activity-dependent manner by increasing the expression of the pro-inflammatory cytokines IL-1alpha, 1beta, 6, 12, 17, TNF-alpha and IFN-gamma. There was also a dose-dependent increase in several growth factors and chemokines following toxin exposure including KC, IL-8, RANTES, and G-CSF. Increased expression of IFN-gamma was observed only in the baboon; otherwise, mice and baboons responded to CARDS toxin in a very similar manner. Introduction of rCARDS toxin to the airways of mice or baboons resulted in a cellular inflammatory response characterized by a dose-dependent early vacuolization and cytotoxicity of the bronchiolar epithelium followed by a robust peribronchial and perivascular lymphocytic infiltration. In mice, rCARDS toxin caused airway hyper-reactivity two days after toxin exposure as well as prolonged airway obstruction. The changes in airway function, cytokine expression, and cellular inflammation correlate temporally and are consistent with what has been reported for M. pneumoniae infection. Altogether, these data suggest that the CARDS toxin interacts extensively with the pulmonary compartment and that the CARDS toxin is sufficient to cause prolonged inflammatory responses and airway dysfunction.
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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.