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Transversal research: neural composition of nasal mucosa of inferior turbinates in patients with allergic rhinitis and non-allergic rhinitis

Grant number: 14/12828-6
Support Opportunities:Regular Research Grants
Duration: April 01, 2015 - March 31, 2017
Field of knowledge:Health Sciences - Medicine
Principal Investigator:João Ferreira de Mello Júnior
Grantee:João Ferreira de Mello Júnior
Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated researchers:Richard Louis Voegels


Allergic rhinitis is a type I hypersensitivity reaction characterized by inflammation dominated eosinophils, immunoglobulin-E mediated and inflammatory mediators responsible for the symptoms. The autonomic nervous system acts in nasal physiology reducing air resistance and increased nasal secretion through its sympathetic and parasympathetic pathways, respectively. The neural functioning of allergic rhinitis, non-allergic of either, is not yet well understood. Some studies suggest the existence of an autonomic imbalance in the idiopathic or vasomotor rhinitis, with inhibition of the sympathetic nervous system in the nose and hyperactivity of the parasympathetic system. In allergic rhinitis occurs also hyperreactivity to nonspecific stimuli. Agents such as odors, pollution and climate change are able to unleash all symptoms of rhinitis without acting directly as allergens. Changes in the structure and function of the nerves (neuronal plasticity) may contribute to the pathophysiology of allergic rhinitis, as well as the response to exogenous and endogenous mediators irritants. Some authors suggest the involvement of neurotrophins in the activation of sensory nerves and the main target cells of the inflammatory response of the upper airway. The main neutrofinas involved in this process are: NGF (nerve growth factor) and BDNF (brain-derived neurotrophic factor). Increasing levels of sodium channels in sensory allergic and non-allergic rhinitis may contribute to the hypersensitive state regardless of the degree of active inflammation. The voltage-dependent sodium channel underlying the generation and propagation of action potentials. Protein gene product 9.5 (PGP 9.5) is a pan-neuronal marker and has been used to demonstrate the presence of neuronal tissues. In allergic rhinitis, the number of nerve fibers PGP 9.5-positive was increased in the epithelium, subepithelium, and mucous glands deeper regions and blood vessels. Recent literature has shown an increase in neural function in the nasal mucosa of people with allergic rhinitis by neurotrophins, nerve fibers and sodium channels, relating to nonspecific hypersensitivity. However, there is a lack of research that relates the amount of these markers with the severity of symptoms and few studies evaluated patients with non-allergic rhinitis. The objective of this study is compare the neuronal activity in the nasal mucosa, through the presence of nerve fibers and neurotrophins, with the intensity of symptoms of rhinitis patients, differentiating allergic and non-allergic individuals. The study will be conducted with 15 patients with allergic rhinitis and 15 patients with non-allergic rhinitis, all of them indicating partial inferior turbinectomy with or without septoplasty. All patients will perform nasal endoscopy, immediate hypersensitivity skin test (prick test) with antigens inhaled and nasal cytology. Tissue samples of inferior turbinate will be submitted to HE staining (hematoxylin-eosin) for quantification of inflammatory cells, mainly eosinophils and mast cells. Immunohistochemistry be done with antibodies to PGP9, 5 (neural marker), NGF, BDNF, NaV1.7, NaV1.8 and NaV1.9. The material collected will be used in the research (Research Protocol n ° 0670/07) "Analysis of the deposition of collagen in the basement membrane of the inferior turbinates in patients with allergic and irritant rhinitis" of performer researcher Daniel Salgado Cauduro and responsible researcher Prof. Dr. Richard Louis Voegels. Immunohistochemical findings will be related to the clinical and compared groups of allergic and non-allergic. (AU)

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