Ozone-Induced Release of Neuropeptides from Human Nasal Mucosa Cells

Schierhorn, Katrin; Hanf, Gerald; Fischer, Axel; Umland, Beate; Kunkel, G.

doi:10.1159/000065879

Cited by 12 publications

(6 citation statements)

References 45 publications

(64 reference statements)

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“…C fibers induce central nervous systemmediated reflexes and also release neuropeptides upon activation, including substance P, neurokinin (NK) A, and calcitionin gene-related peptide (12). Substance P has been shown to be increased in human nasal mucosa and airways after exposure to ozone (13,14).…”

mentioning

confidence: 99%

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Oslund¹,

Hyde

Putney³

et al. 2008

Am J Respir Cell Mol Biol

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We investigated the importance of neurokinin (NK)-1 receptors in epithelial injury and repair and neutrophil function. Conscious Wistar rats were exposed to 1 ppm ozone or filtered air for 8 hours, followed by an 8-hour postexposure period. Before exposure, we administered either the NK-1 receptor antagonist, SR140333, or saline as a control. Ethidium homodimer was instilled into lungs as a marker of necrotic airway epithelial cells. After fixation, whole mounts of airway dissected lung lobes were immunostained for 5-bromo-29-deoxyuridine, a marker of epithelial proliferation. Both ethidium homodimer and 5-bromo-29-deoxyuridine-positive epithelial cells were quantified in specific airway generations. Rats treated with the NK-1 receptor antagonist had significantly reduced epithelial injury and epithelial proliferation compared with control rats. Sections of terminal bronchioles showed no significant difference in the number of neutrophils in airways between groups. In addition, staining ozone-exposed lung sections for active caspase 3 showed no apoptotic cells, but ethidium-positive cells colocalized with the orphan nuclear receptor, Nur77, a marker of nonapoptotic, programmed cell death mediated by the NK-1 receptor. An immortalized human airway epithelial cell line, human bronchial epithelial-1, showed no significant difference in the number of oxidant stresspositive cells during exposure to hydrogen peroxide and a range of SR140333 doses, demonstrating no antioxidant effect of the receptor antagonist. We conclude that activation of the NK-1 receptor during acute ozone inhalation contributes to epithelial injury and subsequent epithelial proliferation, a critical component of repair, but does not influence neutrophil emigration into airways.

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mentioning

confidence: 99%

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Oslund¹,

Hyde

Putney³

et al. 2008

Am J Respir Cell Mol Biol

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“…We have shown that substance P increases acetylcholine release indirectly by activating resident eosinophils and releasing the M 2 receptor antagonist, major basic protein (13). However, ozone increases substance P in airways (27,48,61,62) including in nerve fibers and in nerve cell bodies, that are probably parasympathetic nerve cells, in ferret airways (61). Three days after ozone, when eosinophils are no longer involved in airway hyperreactivity (66), the effectiveness of NK 1 receptor antagonists (Fig.…”

Section: Discussionmentioning

confidence: 90%

Three days after a single exposure to ozone, the mechanism of airway hyperreactivity is dependent on substance P and nerve growth factor

Verhein¹,

Hazari

Moulton

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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Ozone causes persistent airway hyperreactivity in humans and animals. One day after ozone exposure, airway hyperreactivity is mediated by release of eosinophil major basic protein that inhibits neuronal M(2) muscarinic receptors, resulting in increased acetylcholine release and increased smooth muscle contraction in guinea pigs. Three days after ozone, IL-1β, not eosinophils, mediates ozone-induced airway hyperreactivity, but the mechanism at this time point is largely unknown. IL-1β increases NGF and the tachykinin substance P, both of which are involved in neural plasticity. These experiments were designed to test whether there is a role for NGF and tachykinins in sustained airway hyperreactivity following a single ozone exposure. Guinea pigs were exposed to filtered air or ozone (2 parts per million, 4 h). In anesthetized and vagotomized animals, ozone potentiated vagally mediated airway hyperreactivity 24 h later, an effect that was sustained over 3 days. Pretreatment with antibody to NGF completely prevented ozone-induced airway hyperreactivity 3 days, but not 1 day, after ozone and significantly reduced the number of substance P-positive airway nerve bundles. Three days after ozone, NK(1) and NK(2) receptor antagonists also blocked this sustained hyperreactivity. Although the effect of inhibiting NK(2) receptors was independent of ozone, the NK(1) receptor antagonist selectively blocked vagal hyperreactivity 3 days after ozone. These data confirm mechanisms of ozone-induced airway hyperreactivity change over time and demonstrate 3 days after ozone that there is an NGF-mediated role for substance P, or another NK(1) receptor agonist, that enhances acetylcholine release and was not present 1 day after ozone.

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“…This in turn leads to increased plasma excretion and glandular secretion (via acetylcholine and muscarinic receptors) manifesting as pain and stuffiness [29]. Schierhorn et al have shown that ozone increases nasal mucosal levels of SP and neurokinin A (NKA) [30]. NKA is also known to have a similar structure and function to SP, resulting in vascular smooth muscle contraction.…”

Section: Pathogenesismentioning

confidence: 99%

Non-allergic rhinitis: a case report and review

Nozad

Michael

2010

Clin Mol Allergy

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Rhinitis is characterized by rhinorrhea, sneezing, nasal congestion, nasal itch and/or postnasal drip. Often the first step in arriving at a diagnosis is to exclude or diagnose sensitivity to inhalant allergens. Non-allergic rhinitis (NAR) comprises multiple distinct conditions that may even co-exist with allergic rhinitis (AR). They may differ in their presentation and treatment. As well, the pathogenesis of NAR is not clearly elucidated and likely varied. There are many conditions that can have similar presentations to NAR or AR, including nasal polyps, anatomical/mechanical factors, autoimmune diseases, metabolic conditions, genetic conditions and immunodeficiency. Here we present a case of a rare condition initially diagnosed and treated as typical allergic rhinitis vs. vasomotor rhinitis, but found to be something much more serious. This case illustrates the importance of maintaining an appropriate differential diagnosis for a complaint routinely seen as mundane. The case presentation is followed by a review of the potential causes and pathogenesis of NAR.

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Ozone-Induced Release of Neuropeptides from Human Nasal Mucosa Cells

Cited by 12 publications

References 45 publications

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Three days after a single exposure to ozone, the mechanism of airway hyperreactivity is dependent on substance P and nerve growth factor

Non-allergic rhinitis: a case report and review

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