ArticleAmerican journal of respiratory cell and molecular biology2011
Inhibition by cigarette smoke of nuclear factor-κB-dependent response to bacteria in the airway.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- The neuroimmune-glutamate hypothesis of addiction.Neuroscience and biobehavioral reviews · 2026Review
- The radiotherapy induced cyclic GMP-AMP-synthase re-localization and immune signature predicts HNSCC treatment efficacy.Communications medicine · 2026Article
- Conventional, Complementary and Alternative Medicines: Mechanistic Insights into Therapeutic Landscape of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
- Inflammasome involvement in CS-induced damage in HaCaT keratinocytes.In vitro cellular & developmental biology. Animal · 2022Article
- Chronic Obstructive Pulmonary Disease: Epidemiology, Biomarkers, and Paving the Way to Lung Cancer.Journal of clinical medicine · 2021Review
- Particulate air pollution and respiratory Haemophilus influenzae infection in Mianyang, southwest China.Environmental science and pollution research international · 2021Article
- How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression?International journal of chronic obstructive pulmonary disease · 2020Review
- Cigarette smoke preparations, not moist snuff, impair expression of genes involved in immune signaling and cytolytic functions.Scientific reports · 2019Article
- Review
- The Anti-inflammatory Effect of Alpha-1 Antitrypsin in Rhinovirus-infected Human Airway Epithelial Cells.Journal of clinical & cellular immunology · 2016Article
- Cigarette smoke-promoted acquisition of bacterial pathogens in the upper respiratory tract leads to enhanced inflammation in mice.Respiratory research · 2015Article
- In vivo Cigarette Smoke Exposure Decreases CCL20, SLPI, and BD-1 Secretion by Human Primary Nasal Epithelial Cells.Frontiers in psychiatry · 2015Article
- Inflammasome Activity in Non-Microbial Lung Inflammation.Journal of environmental immunology and toxicology · 2014Article
- Molecular processes that drive cigarette smoke-induced epithelial cell fate of the lung.American journal of respiratory cell and molecular biology · 2014Review
- Inflammatory and cytotoxic effects of acrolein, nicotine, acetylaldehyde and cigarette smoke extract on human nasal epithelial cells.BMC pulmonary medicine · 2014Article
- Acrolein exposure suppresses antigen-induced pulmonary inflammation.Respiratory research · 2013Article
- Review
- Cigarette smoking and inflammation: cellular and molecular mechanisms.Journal of dental research · 2012Review
- Cigarette smoke extract (CSE) delays NOD2 expression and affects NOD2/RIPK2 interactions in intestinal epithelial cells.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Although individuals exposed to cigarette smoke are more susceptible to respiratory infection, the effects of cigarette smoke on pulmonary defense are incompletely understood. Based on the observation that interactions between bacteria and host cells result in the expression of critical defense genes regulated by NF-κB, we hypothesized that cigarette smoke alters NF-κB function. In this study, primary human tracheobronchial epithelial cells were treated with cigarette smoke extract (CSE) and exposed to Haemophilus influenzae, and the effects of CSE on bacteria-induced signaling and gene expression were assessed. CSE inhibited high concentrations of induced NF-κB activation and the consequent expression of defense genes that occurred in airway epithelial cells in response to H. influenzae. This decreased activation of NF-κB was not attributable to cell loss or cytotoxicity. Glutathione augmentation of epithelial cells decreased the effects of CSE on NF-κB-dependent responses, as well as the effects on the inhibitor of κB and the inhibitor of κB kinase, which are upstream NF-κB regulators, suggesting the involvement of reactive oxygen species. The relevance of these findings for lung infection was confirmed using a mouse model of H. influenzae airway infection, in which decreased NF-κB pathway activation, keratinocyte chemoattractant (KC) chemokine expression, and neutrophil recruitment occurred in animals exposed to cigarette smoke. The results indicate that although cigarette smoke can cause inflammation in the lung, exposure to smoke inhibits the robust pulmonary defense response to H. influenzae, thereby providing one explanation for the increased susceptibility to respiratory bacterial infection in individuals exposed to cigarette smoke.
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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.