ArticleJournal of neuroinflammation2014
Combustion smoke-induced inflammation in the olfactory bulb of adult rats.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Machine learning approaches to predict maternal anemia and Identifying associated factors among pregnant women in Sub-Saharan Africa.Journal of public health research · 2026Article
- The eNOS isoform exhibits increased expression and activation in the main olfactory bulb of nNOS knock-out mice.Frontiers in cellular neuroscience · 2023Article
- Prevalence and associated factors of severity levels of anemia among women of reproductive age in sub-Saharan Africa: a multilevel ordinal logistic regression analysis.Frontiers in public health · 2023Article
- Effects of nasal inflammation on the olfactory bulb.Journal of neuroinflammation · 2022Review
- Preparation of gastrodin-modified dendrimer-entrapped gold nanoparticles as a drug delivery system for cerebral ischemia-reperfusion injury.Brain and behavior · 2022Article
- Is biomass fuel smoke exposure associated with anemia in non-pregnant reproductive-aged women?PloS one · 2022Article
- Lipopolysaccharide-initiated persistent rhinitis causes gliosis and synaptic loss in the olfactory bulb.Scientific reports · 2017Article
- Acute inhalation of combustion smoke triggers neuroinflammation and persistent anxiety-like behavior in the mouse.Inhalation toxicologyArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 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.
methodsAdult 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.
resultsThe 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).
conclusionsThese 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.
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