ArticleRespiratory research2006
Toll-like receptor-4 mediates cigarette smoke-induced cytokine production by human macrophages.
Article in Respiratory research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00942019 (Bronchial Inflammation in Adolescent Smokers With and Without Obesity), which is not on this map. Cited by 66 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.
The trial behind it
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.
Bronchial Inflammation in Adolescent Smokers With and Without Obesity
Who cites it
66 citing papers in PubMed, 151 citations in OpenAlex.
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- Aged Garlic Extract and Its Bioactive Molecules S-Allyl-Cysteine and S1-Propenyl-Cysteine: A Review Focusing on Evidences Supporting Their Use for Mitigating the Effects of Cigarette Smoking.Molecules (Basel, Switzerland) · 2025Review
- Effects of Smoking on Macrophage Polarization in Peri-Implantitis Lesions.Clinical oral implants research · 2025Article
- Differences in the Inflammatory Response and Corticoid Responsiveness of Human Lung Macrophages and Parenchymal Explants Exposed to Cigarette Smoke Extracts.Basic & clinical pharmacology & toxicology · 2025Article
- Macrophage Polarization and Functions in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Review
- A synbiotic mixture ofFrontiers in nutrition · 2024Article
- Positive association between serum resistin and smoking was strongest in homozygotes of the G-A haplotype at c.-420 C>G and c.-358 G>A in RETN promoter: the Toon Genome Study.Journal of human genetics · 2023Article
- The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis.International journal of molecular sciences · 2023Review
- Review
- Immunoceuticals: Harnessing Their Immunomodulatory Potential to Promote Health and Wellness.Nutrients · 2022Review
- Involvement of the Innate Immune System in the Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2022Review
- Electronic Cigarette Use and the Risk of Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2022Review
- Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Participation of ABCA1 Transporter in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Single Nucleotide Polymorphisms in the Bovine TLR2 Extracellular Domain Contribute to Breed and Species-Specific Innate Immune Functionality.Frontiers in immunology · 2021Article
- The Expression of Toll-Like Receptor 4 mRNA in PBMCs Is Upregulated in Smokers and Decreases Upon Smoking Cessation.Frontiers in immunology · 2021Article
- Toll-Like Receptor-4-Mediated Inflammation is Involved in Intermittent Hypoxia-Induced Lung Injury.Lung · 2020Article
- The Role of Toll-Like Receptors in the Production of Cytokines by Human Lung Macrophages.Journal of innate immunity · 2020Article
- Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe major risk factor for the development of COPD is cigarette smoking. Smoking causes activation of resident cells and the recruitment of inflammatory cells into the lungs, which leads to release of pro-inflammatory cytokines, chemotactic factors, oxygen radicals and proteases. In the present study evidence is found for a new cellular mechanism that refers to a link between smoking and inflammation in lungs.
methodsEmploying human monocyte-derived macrophages, different techniques including FACS analysis, Cytometric Bead Array Assay and ELISA were achieved to evaluate the effects of CS on pro-inflammatory cytokine secretion including IL-8. Then, Toll-like receptor neutralization was performed to study the involvement of Toll-like receptor-4 in IL-8 production. Finally, signaling pathways in macrophages after exposure to CS medium were investigated performing ELISA and Western analysis.
resultsWe demonstrate that especially human monocytes are sensitive to produce IL-8 upon cigarette smoke stimulation compared to lymphocytes or neutrophils. Moreover, monocyte-derived macrophages produce high amounts of the cytokine. The IL-8 production is dependent on Toll-like receptor 4 stimulation and LPS is not involved. Further research resolved the cellular mechanism by which cigarette smoke induces cytokine production in monocyte-derived macrophages. Cigarette smoke causes subsequently a concentration-dependent phosphorylation of IRAK and degradation of TRAF6. Moreover, IkappaBalpha was phosphorylated which suggests involvement of NF-kappaB. In addition, NFkappaB-inhibitor blocked cigarette smoke-induced IL-8 production.
conclusionThese findings link cigarette smoke to inflammation and lead to new insights/therapeutic strategies in the pathogenesis of lung emphysema.
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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.