ArticlePloS one2013
Cigarette smoke decreases airway epithelial FABP5 expression and promotes Pseudomonas aeruginosa infection.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- The role of fatty acid metabolism in acute lung injury: a special focus on immunometabolism.Cellular and molecular life sciences : CMLS · 2024Pooled it
- Fatty acid-binding protein 5 deficiency impairs alveolar macrophage function and metabolism.Journal of lipid research · 2026Article
- 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
- The Biological Functions and Regulatory Mechanisms of Fatty Acid Binding Protein 5 in Various Diseases.Frontiers in cell and developmental biology · 2022Review
- Oxidative stress-induced FABP5 S-glutathionylation protects against acute lung injury by suppressing inflammation in macrophages.Nature communications · 2021Article
- [Effect of intensity of smoking intoxication on severity parameters of acute exacerbations of chronic obstructive pulmonary disease treated in a hospital milieu].The Pan African medical journal · 2021Article
- Changes in salivary proteome before and after cigarette smoking in smokers compared to sham smoking in nonsmokers: A pilot study.Tobacco induced diseases · 2021Article
- The Importance of Metabolism for Immune Homeostasis in Allergic Diseases.Frontiers in immunology · 2021Review
- Fatty acid-binding protein 5 limits ILC2-mediated allergic lung inflammation in a murine asthma model.Scientific reports · 2020Article
- Studying Effects of Cigarette Smoke on Pseudomonas Infection in Lung Epithelial Cells.Journal of visualized experiments : JoVE · 2020Article
- Cigarette smoke extract modulatesAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Particulate matter disrupts airway epithelial barrier via oxidative stress to promoteJournal of thoracic disease · 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
- Smoking-induced iron dysregulation in the lung.Free radical biology & medicine · 2019Review
- Identification of differentially expressed proteins in the injured lung from zinc chloride smoke inhalation based on proteomics analysis.Respiratory research · 2019Article
- The "Iron"-y of Iron Overload and Iron Deficiency in Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2017Article
- Serological Epithelial Component Proteins Identify Intestinal Complications in Crohn's Disease.Molecular & cellular proteomics : MCP · 2017Article
- Cigarette smoke inhibits LPS-induced FABP5 expression by preventing c-Jun binding to the FABP5 promoter.PloS one · 2017Article
- Arylfluorosulfates Inactivate Intracellular Lipid Binding Protein(s) through Chemoselective SuFEx Reaction with a Binding Site Tyr Residue.Journal of the American Chemical Society · 2016Article
- Air pollution particulate matter alters antimycobacterial respiratory epithelium innate immunity.Infection and immunity · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking is the primary cause of Chronic Obstructive Pulmonary Disease (COPD), which is characterized by chronic inflammation of the airways and destruction of lung parenchyma. Repeated and sustained bacterial infections are clearly linked to disease pathogenesis (e.g., exacerbations) and a huge burden on health care costs. The airway epithelium constitutes the first line of host defense against infection and our previous study indicated that Fatty Acid Binding Protein 5 (FABP5) is down regulated in airway epithelial cells of smokers with COPD as compared to smokers without COPD. We hypothesized that cigarette smoke (CS) exposure down regulates FABP5, thus, contributing to a more sustained inflammation in response to bacterial infection. In this report, we show that FABP5 is increased following bacterial infection but decreased following CS exposure of primary normal human bronchial epithelial (NHBE) cells. The goal of this study was to address FABP5 function by knocking down or overexpressing FABP5 in primary NHBE cells exposed to CS. Our data indicate that FABP5 down regulation results in increased P. aeruginosa bacterial load and inflammatory cytokine levels (e.g., IL-8) and decreased expression of the anti-bacterial peptide, β defensin-2. On the contrary, FABP5 overexpression exerts a protective function in airway epithelial cells against P. aeruginosa infection by limiting the production of IL-8 and increasing the expression of β defensin-2. Our study indicates that FABP5 exerts immunomodulatory functions in the airway epithelium against CS exposure and subsequent bacterial infection through its modulation of the nuclear receptor peroxisome proliferator-activated receptor (PPAR)-γ activity. These findings support the development of FABP5/PPAR-γ-targeted therapeutic approach to prevent airway inflammation by restoring antimicrobial immunity during COPD exacerbations.
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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.