ArticleTobacco induced diseases2013
Cigarette smoke extract induces differential expression levels of beta-defensin peptides in human alveolar epithelial cells.
Article in Tobacco induced diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Human beta defensins 3 and 6 serve as diagnostic tools for identifying sepsis and pneumonia.Frontiers in immunology · 2026Article
- Molecular connections between inflammation and social determinants of health.Frontiers in epidemiology · 2025Review
- Article
- Airway microbiome-immune crosstalk in chronic obstructive pulmonary disease.Frontiers in immunology · 2022Review
- Host Defence Peptides in Diabetes Mellitus Type 2 Patients with Periodontal Disease. A Systematic Review.Diagnostics (Basel, Switzerland) · 2021Review
- Epithelial Barrier Dysfunction in Chronic Respiratory Diseases.Frontiers in physiology · 2021Review
- Membrane microdomains regulate NLRP10- and NLRP12-dependent signalling in A549 cells challenged with cigarette smoke extract.Archives of toxicology · 2018Article
- Monocyte-derived exosomes upon exposure to cigarette smoke condensate alter their characteristics and show protective effect against cytotoxicity and HIV-1 replication.Scientific reports · 2017Article
- Human β-defensin 3 increases the TLR9-dependent response to bacterial DNA.European journal of immunology · 2017Article
- Anti-inflammatory effect of Yu-Ping-Feng-SanIranian journal of basic medical sciences · 2016Article
- Effects of Cigarette Smoke Condensate on Oxidative Stress, Apoptotic Cell Death, and HIV Replication in Human Monocytic Cells.PloS one · 2016Article
- Azithromycin attenuates cigarette smoke extract-induced oxidative stress injury in human alveolar epithelial cells.Molecular medicine reports · 2015Article
- Airway β-Defensin-1 Protein Is Elevated in COPD and Severe Asthma.Mediators of inflammation · 2015Article
- Effects of whole cigarette smoke on human beta defensins expression and secretion by oral mucosal epithelial cells.Tobacco induced diseases · 2015Article
- LL-37 secreted by epithelium promotes fibroblast collagen production: a potential mechanism of small airway remodeling in chronic obstructive pulmonary disease.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Comparative study of clinico-bacterio-radiological profile and treatment outcome of smokers and nonsmokers suffering from pulmonary tuberculosis.Lung India : official organ of Indian Chest SocietyArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe damaging effects of cigarette smoke on the lungs are well known in terms of cancer risks. Additional molecular changes within the lung tissue can also occur as a result of exposure to cigarette smoke. The human β-defensin (hBD) class of antimicrobial peptides is the focus of our research. In addition to antimicrobial activity, β-defensins also have immunomodulatory functions. Over 30 previously unrecognized β-defensin genes have recently been identified in the human genome, many with yet to be determined functions. We postulated that altered β-defensin production may play a role in the pathogenesis observed in the lungs of smokers. Our hypothesis is that cigarette smoke exposure will affect the expression of β-defensins in human lung alveolar epithelial cells (A549).
methodsWe exposed A549 cells to cigarette smoke extract (CSE) and measured the changes in mRNA levels of several antimicrobial peptides by quantitative real-time PCR, and directly observed peptide expression in cells by immunofluorescence (IF) microscopy.
resultsWe found that hBD3, hBD5, and hBD9 gene expression was upregulated in A549 cells exposed to CSE. HBD1, hBD8, hBD18 and LL-37 gene expression did not significantly change upon exposure to CSE. Expression of hBD3 and hBD4 peptides was visualized by IF.
conclusionsThis differential expression suggests that hBD3, hBD5, and hBD9 may play a role in the changes to the lung tissue observed in smokers. Establishing differential β-defensin expression following CSE treatment will add to our understanding of the molecular response of the lung alveolar epithelium to 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.