Background: The damaging effect of combustion smoke inhalation on the lung is widely reported but information on its effects on the olfactory bulb is lacking. This study sought to determine the effects of smoke inhalation on the olfactory bulb, whose afferent input neurons in the nasal mucosa are directly exposed to external stimuli, such as smoke.
Methods: Adult male Sprague-Dawley rats were subjected to combustion smoke inhalation and sacrificed at different time points. Changes in olfactory bulb proteins including vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS), Na+-K+-Cl- cotransporter 1 (NKCC1), glial fibrillary acidic protein (GFAP), and aquaporin-4 (AQP4) were evaluated by Western blot analysis. In addition, ELISA was conducted for cytokine and chemokine levels, and double immunofluorescence labeling was carried out for GFAP/VEGF, GFAP/AQP4, NeuN/nNOS, GFAP/NKCC1, NeuN/NKCC1, GFAP/Rhodamine isothiocyanate (RITC), and transferase dUTP nick end labeling (TUNEL). Aminoguanidine was administered to determine the effects of iNOS inhibition on the targets probed after smoke inhalation.
Results: The results showed a significant increase in VEGF, iNOS, eNOS, nNOS, NKCC1, and GFAP expression in the bulb tissues, with corresponding increases in inflammatory cytokines and chemokines after smoke inhalation. Concurrent to this was a drastic increase in AQP4 expression and RITC permeability. Aminoguanidine administration decreased the expression of iNOS and RITC extravasation after smoke inhalation. This was coupled with a significant reduction in incidence of TUNEL + cells that was not altered with administration of L-NG-nitroarginine methyl ester (L-NAME).
Conclusions: These findings suggest that the upregulation of iNOS in response to smoke inhalation plays a major role in the olfactory bulb inflammatory pathophysiology, along with a concomitant increase in pro-inflammatory molecules, vascular permeability, and edema. Overall, these findings indicate that the olfactory bulb is vulnerable to smoke inhalation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197300 | PMC |
| http://dx.doi.org/10.1186/s12974-014-0176-5 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Inhalation of patchouli essential oil alleviates airway inflammation in cigarette smoke-induced COPD mice.
Sci Rep
December 2024
State Key Laboratory of Biobased Material and Green Papermaking, School of Bioengineering, Qilu University of Technology, Shandong Academy of Sciences, Jinan, People's Republic of China.
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, characterized by persistent respiratory symptoms and airflow limitations resulting from small airway injury, bronchial wall thickening, and hypersecretion of mucus. Current pharmacological interventions are ineffective in reversing these airflow limitations; In our study, we investigated the potential role of patchouli essential oil (PEO) in the treatment of COPD and its underlying molecular mechanisms, both in vitro and in vivo. To establish a cigarette smoke-induced COPD mice model, we exposed the mice to cigarette smoke (CS) and administered nasal drip of lipopolysaccharides (LPS).
View Article and Find Full Text PDFA New Perspective for Improving COPD: Ginsenoside Rg3 Links SIRT1 to Inhibit Mitochondrial Autophagy.
Discov Med
December 2024
Department of Respiratory Medicine, The First Affiliated Hospital of Anhui University of Chinese Medicine, 230031 Hefei, Anhui, China.
Background: Chronic obstructive pulmonary disease (COPD) is a prevalent yet manageable respiratory condition. However, treatments presently used normally have side effects and cannot cure COPD, making it urgent to explore effective medications. The ginsenoside Rg3 (Rg3) has been shown to have anti-inflammatory and anti-tumor properties and can improve COPD.
View Article and Find Full Text PDFAssociation Between Incense Burning and the Risk of Lung Cancer in Asian Population: Meta-Analysis of Nine Case-Control Studies.
Cancer Rep (Hoboken)
December 2024
Faculty of Resource Science and Technology, University Malaysia Sarawak, Kota Samarahan, Malaysia.
Background: Various studies have explored the potential association between incense burning and the risk of lung cancer. However, the findings from these studies have been inconsistent.
Objectives: This study aimed to provide a more comprehensive understanding of the relationship between incense burning and lung cancer risk in the Asian population through a meta-analysis.
TRPA1 contributes to respiratory depression from tobacco aerosol.
Respir Physiol Neurobiol
December 2024
Department of Physiology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan. Electronic address:
Transient receptor potential ankyrin-1 (TRPA1) is expressed in the trigeminal nerves in the nasal cavity. It detects irritant chemicals such as formalin and acrolein, induces respiratory depression to protect against further inhalation, and elicits avoidance behavior. Although tobacco smoke contains formalin, acrolein, and other irritant chemicals, the possible contribution of TRPA1 to protection against tobacco smoke has yet to be fully understood.
View Article and Find Full Text PDFChemical burns account for a small percentage of burn patients, and there are even fewer burn patients suffering from chemical burns combined with inhalation injury. As chemical substances corrode the airway, which leads to persistent necrotic shedding of the respiratory mucosa and scarring contracture as the airway heals, a proportion of patients develop airway stenosis, requiring more aggressive treatment or even surgery. A 38-year-old female chemical factory worker sustained an inhalation injury due to exposure to reactive substances (liquid and smoke) during production.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!