ArticleInternational immunopharmacology2010
Inactivation of I kappaB-kinase-beta dependent genes in airway epithelium reduces tobacco smoke induced acute airway inflammation.
Article in International immunopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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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.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Medicinal Foods, YT and RH Combination, Suppress Cigarette Smoke-Induced Inflammation and Oxidative Stress by Inhibiting NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The adverse impact of cadmium on immune function and lung host defense.Seminars in cell & developmental biology · 2021Article
- Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases: A Mechanistic Review.International journal of environmental research and public health · 2018Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
We have examined the role of NF-kappaB regulated genes in airway epithelium in mediating tobacco smoke induced airway inflammation in studies of CC10-Cre(tg)/Ikk beta(Delta/Delta) mice in which NF-kappaB signaling through I kappaB-kinase-beta (IKK-beta) is selectively ablated in epithelial cells in the airway. CC10-Cre(tg)/Ikk beta(Delta/Delta) mice exposed to tobacco smoke for seven days had a significant decrease in the number of BAL cells (total cells, neutrophils, and macrophages) as well as significantly reduced numbers of peribronchial cells (F4/80+ and myeloperoxidase+) compared to tobacco exposed WT mice. In addition to the reduction in peribronchial cells, CC10-Cre(tg)/Ikk beta(Delta/Delta) mice exposed to tobacco smoke had a significant decrease in the number of macrophages and neutrophils in the alveolar space suggesting that inactivation of NF-kappaB in the airway epithelium influenced the number of neutrophils and macrophages recruited to the alveolus. Levels of the NF-kappaB regulated chemokines KC and MCP-1 were significantly reduced in lungs of tobacco smoke exposed CC10-Cre(tg)/Ikk beta(Delta/Delta) mice compared to tobacco exposed WT mice. In contrast, there was no significant difference in levels of NF-kappaB regulated MIP-1 alpha between CC10-Cre(tg)/Ikk beta(Delta/Delta) and WT mice. Lung sections of tobacco smoke exposed CC10-Cre(tg)/Ikk beta(Delta/Delta) mice immunostained with KC or MCP-1 antibodies demonstrated reduced expression of these chemokines in the airway epithelium, but not in alveolar epithelium. Overall, these studies demonstrate an important role for NF-kappaB regulated genes in airway epithelium in contributing to acute tobacco smoke induced airway inflammation not only in the peribronchial space but also in the alveolar space.
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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.