ArticleInfection and immunity2014
Cytadherence of Mycoplasma pneumoniae induces inflammatory responses through autophagy and toll-like receptor 4.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- The role of the PM2.5-associated metals in pathogenesis of child Mycoplasma Pneumoniae infections: a systematic review.Environmental science and pollution research international · 2016Pooled it
- Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.European journal of pediatrics · 2026Review
- Pathogenesis and Risk Factors of Post-Infectious Bronchiolitis Obliterans in Children: A Focus on Adenovirus and Mycoplasma Infections.Pathogens (Basel, Switzerland) · 2026Review
- Mucositis Associated withChildren (Basel, Switzerland) · 2026Review
- 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
- Pro-Inflammatory Response of Bovine Lung Explant Induced byPathogens (Basel, Switzerland) · 2026Article
- AgeFrontiers in pediatrics · 2026Article
- Advances in adhesion-related pathogenesis inFrontiers in microbiology · 2025Review
- Predictive value of plasma sB7-H3 and YKL-40 in pediatric refractory Mycoplasma pneumoniae pneumonia.Open medicine (Warsaw, Poland) · 2025Article
- Exploring the pathogenetic mechanisms ofExperimental and therapeutic medicine · 2024Review
- Aerobic glycolysis of bronchial epithelial cells rewiresInfection and immunity · 2024Article
- Insights into the defensive roles of lncRNAs duringFrontiers in microbiology · 2024Review
- Identification ofFrontiers in microbiology · 2024Article
- Proteomic and Phenotypic Studies of Mycoplasma pneumoniae Revealed Macrolide-Resistant Mutation (A2063G) Associated Changes in Protein Composition and Pathogenicity of Type I Strains.Microbiology spectrum · 2023Article
- Extracellular Vesicles Released from Macrophages Infected withInternational journal of molecular sciences · 2023Article
- Potential Therapeutic Value of the STING Inhibitors.Molecules (Basel, Switzerland) · 2023Review
- The Role of Macrophage Autophagy in Asthma: A Novel Therapeutic Strategy.Mediators of inflammation · 2023Review
- The first Mycoplasma ovipneumoniae recovered from a sheep with respiratory disease in Brazil - draft genome and genomic analysis.Veterinary research communications · 2022Article
- Development of a model for early differentiation of adenovirus pneumonia fromTranslational pediatrics · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycoplasma pneumoniae causes pneumonia, tracheobronchitis, pharyngitis, and asthma in humans. The pathogenesis of M. pneumoniae infection is attributed to excessive immune responses. We previously demonstrated that M. pneumoniae lipoproteins induced inflammatory responses through Toll-like receptor 2 (TLR2). In the present study, we demonstrated that M. pneumoniae induced strong inflammatory responses in macrophages derived from TLR2 knockout (KO) mice. Cytokine production in TLR2 KO macrophages was increased compared with that in the macrophages of wild-type (WT) mice. Heat-killed, antibiotic-treated, and overgrown M. pneumoniae failed to induce inflammatory responses in TLR2 KO macrophages. 3-Methyladenine and chloroquine, inhibitors of autophagy, decreased the induction of inflammatory responses in TLR2 KO macrophages. These inflammatory responses were also inhibited in macrophages treated with the TLR4 inhibitor VIPER and those obtained from TLR2 and TLR4 (TLR2/4) double-KO mice. Two mutants that lacked the ability to induce inflammatory responses in TLR2 KO macrophages were obtained by transposon mutagenesis. The transposons were inserted in atpC encoding an ATP synthase F0F1 ε subunit and F10_orf750 encoding hypothetical protein MPN333. These mutants showed deficiencies in cytadherence. These results suggest that cytadherence of M. pneumoniae induces inflammatory responses through TLR4 and autophagy.
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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.