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Project

Exploring the neuro-immune mechanisms underlying nasal hyperreactivity in rhinitis and rhinosinusitis

Rhinitis can present with nasal obstruction, nasal discharge, itch, or sneezing. In case of involvement of the paranasal sinuses (i.e. rhinosinusitis), facial pain or loss of smell is possible as well. Several endotypes of rhinitis and rhinosinusitis are known, such as type 1 or type 2 inflammation.

Allergic rhinitis (AR) and chronic rhinosinusitis with nasal polyps (CRSwNP) are both characterized by a mainly type 2 inflammation in the Western population. Nasal hyperreactivity (NHR), defined as the induction of nasal symptoms upon encounter of environmental stimuli, has a self-reported prevalence of 58% and 41% in AR and CRSwNP respectively. In non-allergic rhinitis, over-expression of particular thermosensitive, chemonociceptive receptors on afferent nerves (TRPV1, TRPVA1) makes the mucosa more sensitive to external triggers, hence leading to NHR. However, the pathophysiology of NHR in AR and CRSwNP is incompletely understood.

In this project, we want to elude the mechanisms underlying NHR in AR and CRSwNP, offering new therapeutic perspectives. We hypothesize that neuropeptides (substance P) and mast cell mediators (histamine) induce NHR by influencing TRPV1, TRPA1 or TRPM8. Therefore, we will investigate which mediators are present in the nasal secretions of patients with NHR and how they influence the TRP-channels on murine trigeminal neurons. At last, we will test our hypothesis in vivo in a house dust mite-allergic mouse model using a cold, dry air provocation test.

Date:1 Sep 2018 →  20 Sep 2022
Keywords:Nasal hyperreactivity, Allergic rhinitis, Chronic rhinosinusitis
Disciplines:Immunology
Project type:PhD project