ArticlePloS one2009
Impact of cigarette smoke exposure on innate immunity: a Caenorhabditis elegans model.
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 21 papers, 2 of them syntheses that pooled it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.
- Smoking and multiple sclerosis: an updated meta-analysis.PloS one · 2011Pooled it
- Association of secondhand smoke exposure with pediatric invasive bacterial disease and bacterial carriage: a systematic review and meta-analysis.PLoS medicine · 2010Pooled it
- Fatty acid-binding protein 5 deficiency impairs alveolar macrophage function and metabolism.Journal of lipid research · 2026Article
- Heated tobacco and cigarette smoke modulate CD4 + T cell activation and neuroinflammation in a context-dependent manner.Journal of neuroinflammation · 2026Article
- In vitro modelling of bacterial pneumonia: a comparative analysis of widely applied complex cell culture models.FEMS microbiology reviews · 2024Review
- Macrophage programming is regulated by a cooperative interaction between fatty acid binding protein 5 and peroxisome proliferator-activated receptor γ.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Why new biology must be uncovered to advance therapeutic strategies for chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2021Review
- Cigarette smoke extract modulatesAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Combustible Cigarette and Smokeless Tobacco Product Preparations Differentially Regulate Intracellular Calcium Mobilization in HL60 Cells.Inflammation · 2019Article
- Air Pollution Alters Caenorhabditis elegans Development and Lifespan: Responses to Traffic-Related Nanoparticulate Matter.The journals of gerontology. Series A, Biological sciences and medical sciences · 2019Article
- Impact of fatty acid binding protein 5-deficiency on COPD exacerbations and cigarette smoke-induced inflammatory response to bacterial infection.Clinical and translational medicine · 2019Article
- Induction of Metallothionein Expression After Exposure to Conventional Cigarette Smoke but Not Electronic Cigarette (ECIG)-Generated Aerosol inFrontiers in physiology · 2018Article
- Global Proteomics RevealedFrontiers in cellular and infection microbiology · 2017Article
- Cigarette smoke inhibits LPS-induced FABP5 expression by preventing c-Jun binding to the FABP5 promoter.PloS one · 2017Article
- C. elegans and mutants with chronic nicotine exposure as a novel model of cancer phenotype.Cancer biology & therapy · 2016Article
- A C. elegans model of electronic cigarette use: Physiological effects of e-liquids in nematodes.BMC pharmacology & toxicology · 2015Article
- Animals devoid of pulmonary system as infection models in the study of lung bacterial pathogens.Frontiers in microbiology · 2015Review
- FABP5 deficiency enhances susceptibility to H1N1 influenza A virus-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Cigarette smoke decreases airway epithelial FABP5 expression and promotes Pseudomonas aeruginosa infection.PloS one · 2013Article
- Cigarette smoke inhibits airway epithelial cell innate immune responses to bacteria.Infection and immunity · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCigarette smoking is the major cause of chronic obstructive pulmonary disease (COPD) and lung cancer. Respiratory bacterial infections have been shown to be involved in the development of COPD along with impaired airway innate immunity. METHODOLOGY/PRINCIPAL
findingsTo address the in vivo impact of cigarette smoke (CS) exclusively on host innate defense mechanisms, we took advantage of Caenorhabditis elegans (C. elegans), which has an innate immune system but lacks adaptive immune function. Pseudomonas aeruginosa (PA) clearance from intestines of C. elegans was dampened by CS. Microarray analysis identified 6 candidate genes with a 2-fold or greater reduction after CS exposure, that have a human orthologue, and that may participate in innate immunity. To confirm a role of CS-down-regulated genes in the innate immune response to PA, RNA interference (RNAi) by feeding was carried out in C. elegans to inhibit the gene of interest, followed by PA infection to determine if the gene affected innate immunity. Inhibition of lbp-7, which encodes a lipid binding protein, resulted in increased levels of intestinal PA. Primary human bronchial epithelial cells were shown to express mRNA of human Fatty Acid Binding Protein 5 (FABP-5), the human orthologue of lpb-7. Interestingly, FABP-5 mRNA levels from human smokers with COPD were significantly lower (p = 0.036) than those from smokers without COPD. Furthermore, FABP-5 mRNA levels were up-regulated (7-fold) after bacterial (i.e., Mycoplasma pneumoniae) infection in primary human bronchial epithelial cell culture (air-liquid interface culture).
conclusionsOur results suggest that the C. elegans model offers a novel in vivo approach to specifically study innate immune deficiencies resulting from exposure to cigarette smoke, and that results from the nematode may provide insight into human airway epithelial cell biology and cigarette smoke exposure.
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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.