Non allergic rhinitis (NAR)
Non allergic rhinitis in children is poorly defined [26]. Previously
AR was clearly discriminated by NAR by means of increased local
total/local IgE specific levels and nasal eosinophils and these
differences were more pronounced in children than adults with AR,
suggesting that AR in children is a more distinct feature [27].
However, inflammatory mediators related to different inflammatory
endotypes detected from nasal cytology cannot discriminate AR from NAR
adult patients [28].
Local allergic rhinitis (LAR) in children is an emerging
disease, highly underdiagnosed [29]. Increased levels of local IgE
in the nasal lavage fluid has been proposed as a useful biomarker in
children with suspected LAR [30]. Local production of “T2”
inflammatory mediators has been demonstrated following nasal allergen
challenges in a pediatric setting [31]. Nevertheless, AR and LAR
share several clinical and immune features, such as positive response to
a nasal allergen provocation test, increased risk of asthma occurrence
and increased nasal IgE production [32]. Moreover, the
FcepsilonR1beta genetic polymorphism has been linked both with LAR and
AR prevalence [33].
Nasal hyperreactivity (NHR) constitutes a cardinal
clinical feature both in AR and NAR [34] and has been previously
documented in children with allergic rhinitis, although respective
techniques are difficult to apply in clinical use and young ages [35,
36]. The most well described pathogenetic mechanism involves a
“dysregulated” neural innervation network. In NAR and NHR, the role of
the efferent component via the activated transient receptor potential
(TRP) ion channels (receptor 1_TRPA1 and subfamily V-TRPV1), induces
the release of neuropeptides, such as CGRP and substance P (SP),
neurokinin A and B from sensory nerve endings, which in turn induce
sneezing, mucus production and congestion [37]. In line,
histological data are indicative of increased expression of the
aforementioned neuropeptides of the nasal mucosa in patients with NHR
and NAR [38]. Moreover, the impact of environmental and microbial
factors (i.e.; staphylococcus Aureus enterotoxins) has been postulated
for triggering local nerve endings, more so in the presence of a
disrupted epithelium barrier [39]. It remains to be elucidated
whether barrier dysfunction is a primary (genetic) defect or secondary
to infectious agents or allergens [40, 41].