Non-Allergic Rhinitis with Eosinophils and Mast Cells Constitutes a New Severe Nasal Disorder

Gelardi, Matteo; Giudice, Alessandro Maselli Del; Fiorella, Maria Luisa; Fiorella, R; Russo, Cosimo Roberto; Soleti, P.; Gioacchino, Mario Di; Ciprandi, Giorgio

doi:10.1177/039463200802100209

Cited by 71 publications

(71 citation statements)

References 16 publications

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“…In the present study, we show that stimulation of SCCs triggers a proinflammatory pathway reflecting common features with idiopathic NAR (11,(48)(49)(50). Patients with NAR, similar to patients afflicted with asthma or chronic obstructive pulmonary disease (COPD), report hyperresponsiveness to normally benign odorants (51), including many chemicals that activate SCCs (52).…”

Section: Related To Nonallergic Rhinitis (Nar)mentioning

confidence: 74%

Cholinergic neurotransmission links solitary chemosensory cells to nasal inflammation

Saunders

Christensen

Finger

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

182

233

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Solitary chemosensory cells (SCCs) of the nasal cavity are specialized epithelial chemosensors that respond to irritants through the canonical taste transduction cascade involving Gα-gustducin and transient receptor potential melastatin 5. When stimulated, SCCs trigger peptidergic nociceptive (or pain) nerve fibers, causing an alteration of the respiratory rate indicative of trigeminal activation. Direct chemical excitation of trigeminal pain fibers by capsaicin evokes neurogenic inflammation in the surrounding epithelium. In the current study, we test whether activation of nasal SCCs can trigger similar local inflammatory responses, specifically mast cell degranulation and plasma leakage. The prototypical bitter compound, denatonium, a well-established activator of SCCs, caused significant inflammatory responses in WT mice but not mice with a genetic deletion of elements of the canonical taste transduction cascade, showing that activation of taste signaling components is sufficient to trigger local inflammation. Chemical ablation of peptidergic trigeminal fibers prevented the SCC-induced nasal inflammation, indicating that SCCs evoke inflammation only by neural activity and not by release of local inflammatory mediators. Additionally, blocking nicotinic, but not muscarinic, acetylcholine receptors prevents SCC-mediated neurogenic inflammation for both denatonium and the bacterial signaling molecule 3-oxo-C12-homoserine lactone, showing the necessity for cholinergic transmission. Finally, we show that the neurokinin 1 receptor for substance P is required for SCC-mediated inflammation, suggesting that release of substance P from nerve fibers triggers the inflammatory events. Taken together, these results show that SCCs use cholinergic neurotransmission to trigger peptidergic trigeminal nociceptors, which link SCCs to the neurogenic inflammatory pathway.rhinitis | innate immunity | quorum sensing | chemesthesis | airway irritation

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Section: Related To Nonallergic Rhinitis (Nar)mentioning

confidence: 74%

Cholinergic neurotransmission links solitary chemosensory cells to nasal inflammation

Saunders

Christensen

Finger

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

182

233

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“…Although it is controversial on how to best subdivide NAR, several studies have recently demonstrated that a cytological approach may be useful not only to establish involvement of inflammation, but also to improve classification (19)(20)(21) . There is debate regarding the role of inflammation in NAR.…”

Section: Introductionmentioning

confidence: 99%

Role of inflammation in non-allergic rhinitis

Corso¹,

Battista²,

Pandolfini³

et al. 2014

Rhin

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Objective: To investigate the role of inflammation in non-allergic rhinitis (NAR) patients in a large series to establish the prevalence of different NAR-subtypes, clinical features and the role of nasal cytology in the diagnostic algorithm. Methodology:Patients were selected out of 3650 individuals who spontaneously presented at our institution. We consecutively enrolled 519 NAR-patients in an analytical cross-sectional study between November 2007 and June 2013 (level of evidence: 3b).All patients underwent rhinological evaluation including symptoms questionnaire, endoscopy, CT scan, allergy tests and nasal cytology. Results:The inflammatory cell infiltrate affects the severity of symptoms differently, allowing for identification of different phenotypes of NAR. We distinguished two groups: "NAR without inflammation"(NAR-) and "NAR with inflammation"(NAR+), in addition to different NAR-subtypes with inflammation. A significant difference was observed in terms of clinical symptoms and association with comorbidities (previously diagnosed asthma and aspirin intolerance) between NAR-, NAR+ and between different NAR+ subtypes. Conclusion:Our data suggest that NAR-and NAR with neutrophils behave similarly, showing lower symptom score values and a lower risk of association with comorbidities compared to NAR with eosinophils and mast cells (singularly or mixed). In our belief it is very important to establish the presence and type of inflammation in non-allergic rhinitis patients and nasal cytology is a very useful test in correct differential diagnosis.

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“…Findings also support the view that neuro-immune abnormalities occur in the brain of autistic patients and may contribute to the diversity of the autistic phenotypes (4). Although several lines of research support the view that this is a result of a complex combination of neurological, environmental, immunological, and genetic factors, it is widely reported that several white blood cells are important in the pathogenesis of neurological diseases (5)(6)(7)(8), and it is established in animal and human diseases such as autoimmunity, inflammation and cancer (9)(10)(11)(12)(13)(14). In addition, proinflammatory cytokines secreted by different types of cells contribute to the pathogenesis ofneuro-inflammation (12,15).…”

mentioning

confidence: 99%

Autism and Immunity: Revisited Study

Castellani

Conti

Kempuraj

et al. 2009

Int J Immunopathol Pharmacol

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Autism spectrum disorder is of interest neurochemically because it represents a relatively homogeneous disorder with regard to disease development, abnormal cognitive development and intellectual development disturbance. A consistent finding in autistic children is a high number of mast cells and a high level of serotonin which is also found at elevated concentrations in the urine of autistic patients. In addition, a dysfunction of clinical conditions, such as gastrointestinal and immunological symptoms, is frequently noted in autistic children, however, IgE does not appear to be prevalent in these children but probably an increase of cytokines/chemokines produced by mast cells at an early age may play an important role. Therefore an immune hypothesis, involving also autoimmunity, is one possible pathogenetic mechanism in autism. In conclusion, mast cell activation could contribute to immune and neuroinflammatory abnormalities that are evident in patients with autism spectrum disorders.Autism and autism spectrum disorders are complex neuro-developmental disorders characterized by disturbance and impairments in social skills and interaction, verbal communication,

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Non-Allergic Rhinitis with Eosinophils and Mast Cells Constitutes a New Severe Nasal Disorder

Cited by 71 publications

References 16 publications

Cholinergic neurotransmission links solitary chemosensory cells to nasal inflammation

Cholinergic neurotransmission links solitary chemosensory cells to nasal inflammation

Role of inflammation in non-allergic rhinitis

Autism and Immunity: Revisited Study

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