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.
Highlights
The damaging effect of combustion smoke inhalation on the lung is widely reported but information on its effects on the olfactory bulb is lacking
Elevated inflammatory cytokines after smoke inhalation In the olfactory bulb tissue, the concentration levels of the cytokines IL-1α, interleukin-1 β (IL-1β), IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, IFN-γ, tumor necrosis factor-α (TNF-α), GM-CSF, and RANTES were increased significantly at 24 h in the SI + S group when compared with the matched control (Figure 2)
The present findings suggest that the upregulation of inducible nitric oxide synthase (iNOS) in response to smoke inhalation plays a major role in olfactory bulb inflammatory pathophysiology after smoke inhalation, with concomitant increases in pro-inflammatory molecules, vascular permeability, and edema
Summary
The damaging effect of combustion smoke inhalation on the lung is widely reported but information on its effects on the olfactory bulb is lacking. The olfactory bulb participates in many physiological functions, such as appetite regulation, lactation, response to adverse environments, and social interaction [2,3]. It contains a large number of afferent input sensory cells that might be. Smoke inhalation injury has been reported to lead to a 20% increase in mortality in burn patients. In conjunction with such comorbidities as pneumonia, mortality can further increase by up to 60%
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