ArticleClinical and experimental immunology2021
Mycoplasma pneumoniae lipids license TLR-4 for activation of NLRP3 inflammasome and autophagy to evoke a proinflammatory response.
Article in Clinical and experimental immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 56 citations in OpenAlex.
- Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.European journal of pediatrics · 2026Review
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- Pathogenesis and Risk Factors of Post-Infectious Bronchiolitis Obliterans in Children: A Focus on Adenovirus and Mycoplasma Infections.Pathogens (Basel, Switzerland) · 2026Review
- Investigation of transcription factor NFκB-mediated autophagy regulation mechanisms in non-small cell lung cancer.Molecular biology reports · 2026Article
- MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy.Frontiers in pediatrics · 2026Article
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- Comparative progress on the mechanisms of airway mucosal injury induced by different pathogens: SARS-CoV-2, influenza A virus, and Mycoplasma pneumoniae.Frontiers in cellular and infection microbiology · 2026Review
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- Role of P38 lipoprotein in Mycoplasma penetrans adhesion to human urothelial cells.BMC microbiology · 2025Article
- Unraveling the role of distinct cytoskeletal motility structures in Mycoplasma pneumoniae relatives.BMC microbiology · 2025Review
- MreB: unraveling the molecular mechanisms of bacterial shape, division, and environmental adaptation.Cell communication and signaling : CCS · 2025Review
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- [Protective effect ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Exploring the pathogenetic mechanisms ofExperimental and therapeutic medicine · 2024Review
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- Aerobic glycolysis of bronchial epithelial cells rewiresInfection and immunity · 2024Article
- Yinqin Qingfei granules alleviateFrontiers in pharmacology · 2024Article
- Roles of MDA-LDL/OX-LDL/LOX-1 and TNF-α/TLR4/NF-κB Signaling Pathways in Myocardial Damage by Implantations of Cardiac Pacemakers in Elderly Patients.Current vascular pharmacology · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycoplasma pneumoniae is an obligate pathogen that causes pneumonia, tracheobronchitis, pharyngitis and asthma in humans. It is well recognized that membrane lipoproteins are immunostimulants exerting as lipopolysaccharides (LPS) and play a crucial role in the pathogenesis of inflammatory responses upon M. pneumoniae infection. Here, we report that the M. pneumoniae-derived lipids are another proinflammatory agents. Using an antibody-neutralizing assay, RNA interference or specific inhibitors, we found that Toll-like receptor 4 (TLR-4) is essential for M. pneumoniae lipid-induced tumour necrosis factor (TNF)-α and interleukin (IL)-1β production. We also demonstrate that NLR family pyrin domain containing 3 inflammasome (NLRP3) inflammasome, autophagy and nuclear factor kappa B (NF-κB)-dependent pathways are critical for the secretion of proinflammatory cytokines, while inhibition of TLR-4 significantly abrogates these events. Further characterization revealed that autophagy-mediated inflammatory responses involved the activation of NF-κB. In addition, the activation of NF-κB promoted lipid-induced autophagosome formation, as revealed by assays using pharmacological inhibitors, 3-methyladenine (3-MA) and Bay 11-7082, or silencing of atg5 and beclin-1. These findings suggest that, unlike the response to lipoprotein stimulation, the inflammation in response to M. pneumoniae lipids is mediated by the TLR-4 pathway, which subsequently initiates the activation of NLRP3 inflammasome and formation of a positive feedback loop between autophagy and NF-κB signalling cascade, ultimately promoting TNF-α and Il-1β production in macrophages.
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