Important roles of tachykinins in the development of allergic nasal hyperresponsiveness in guinea‐pigs

Abstract

SP and NKA, which are released early after the challenge, mediate the development of NHR by preferentially activating NK(2) receptors. Therefore, NK(2) receptor antagonists might prove to be effective treatment of AR.

Contribution of Neurogenic and Allergic Ways to the Pathophysiology of Nonallergic Rhinitis

“…Both neurogenic and allergic ways seem to play a role in the early nasal hyperreactivity of NAR, like in AR. This may be explained by the neuroallergic interaction of substance p and histamine stimulating the release of each other [12,13,24,25]. In conclusion, we can explain the similarities between NAR and AR including nasal symptoms, nasal hyperreactivity to allergen and nasal inflammation by the common mechanism of neuroallergy, whereas the differences between these rhinitis types may be attributed to the different contribution of neurogenic and allergic ways.…”

“…We did not assess late allergic response, reported to be present in low ratios in AR as well as in NAR, but only if it was accompanied by early response [5,20,22]. Furthermore, the neurogenic way was shown to only evoke early nasal reaction, and substance p was found to be released early after the challenge [12,20]. …”

“…It was reported that substance p was released early after allergen challenge and mediated the development of nasal hyperreactivity in patients with AR, but without response in the normal nose [14]. Furthermore, in contrast to sensitized/challenged animals, non-sensitized guinea pigs did not exhibit nasal hyperreactivity after NPT with substance p [12]. However, substance p was also found in the nasal mucosa of NAR patients, as much as in AR patients, but with less inflammation [15].…”

“…Substance p is a neuropeptide released from the sensory nerves of the upper respiratory tract and stimulates ‘neurogenic inflammation’ by inducing glandular secretion, plasma leakage, vasodilatation, cholinergic activation, and inflammatory cell infiltration with its receptors on sensory neurons, mucosal glands, epithelial and inflammatory cells [11,12,13]. As allergens increase the amount of neuropeptide production by histamine receptors on sensory nerves [14], neurotransmitters also induce histamine release by mast cell degranulation [12,13,14]. The interaction of neurogenic and allergic mechanisms may be renamed the ‘neuroallergic way’.…”

Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis

“…In the guinea pig model of allergic rhinitis, the sneezing reflex following allergen challenge is inhibited significantly by pretreatment with capsaicin, which depletes SP and CGRP from the nasal mucosa [28]. When various chemical mediators are applied to the nasal mucosa, histamine is the only mediator that induces a significant sneezing reflex [28,29]. Therefore, the sneezing reflex following allergen challenge is a respiratory reflex induced by the interaction between histamine and the H1 receptor at the sensory nerve terminals containing SP and CGRP and might be a sensory stimulation response amplified by hyperreactivity in the nasal mucosa [25].…”