Neuropeptide immunofluorescence in human nasal mucosa: assessment of the technique for vasoactive intestinal peptide (VIP)

Mendonça, Jeferson Cedaro de; Dolci, José Eduardo Lutaif

doi:10.1016/s1808-8694(15)31299-4

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…Presumably this breath-holding response exists to limit further inhalation of toxic compounds. As trigeminal nociceptors also express and release several types of signaling neuropeptides into the local environment, including vasoactive intestinal peptide, substance P, and calcitonin gene-related peptide, [97][98][99][100][101] it is likely that SCC activation also results in local responses, which may include blood vessel dilation and/or inflammation, 97,[102][103][104][105] enhanced ciliary beating, 8 or fluid secretion from submucosal exocrine glands. 23,[106][107][108] However, these effects remain to be experimentally confirmed.…”

Section: Nasal Solitary Chemosensory Cells-discovery and Initial Characterization In Micementioning

confidence: 99%

Sinonasal Solitary Chemosensory Cells “Taste” the Upper Respiratory Environment to Regulate Innate Immunity

Lee

Cohen

2014

Am J Rhinol�Allergy

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SCCs appear to be important mediators of upper airway innate immunity, as the SCC T2Rs regulate antimicrobial peptide secretion, but further study is needed to determine the specific T2R isoforms involved as well as whether polymorphisms in these isoforms affect susceptibility to infection or patient outcomes in CRS. The inhibitory role of T1R2/3 sweet receptor suggests that T1R2/3 blockers may have therapeutic potential in some CRS patients, particularly those with diabetes mellitus. However, further clinical study of the relationship between infection and T1R2/3 genotype is required.

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Section: Nasal Solitary Chemosensory Cells-discovery and Initial Characterization In Micementioning

confidence: 99%

Sinonasal Solitary Chemosensory Cells “Taste” the Upper Respiratory Environment to Regulate Innate Immunity

Lee

Cohen

2014

Am J Rhinol�Allergy

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“…5-7), which regulates vasodilation, mucus secretion, and immune modulation (8 -10). Parasympathetic VIPergic neurons exist throughout the sinonasal epithelium (8,9,(11)(12)(13)(14)(15)(16)(17)(18), and VIP receptors are expressed on sinonasal epithelial and gland cells (8, 9, 19 -23). It is thought that VIP activates receptor-linked G␣ s and downstream adenylyl and/or guanylyl cyclase activation, resulting in stimulation of cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) and/or cGMP-dependent protein kinase G (PKG) (24 -26).…”

mentioning

confidence: 99%

Vasoactive intestinal peptide regulates sinonasal mucociliary clearance and synergizes with histamine in stimulating sinonasal fluid secretion

et al. 2013

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Mucociliary clearance (MCC) is the primary physical airway defense against inhaled pathogens and particulates. MCC depends on both proper fluid/mucus homeostasis and epithelial ciliary beating. Vasoactive intestinal peptide (VIP) is a neurotransmitter expressed in the sinonasal epithelium that is up-regulated in allergy. However, the effects of VIP on human sinonasal physiology are unknown, as are VIP's interactions with histamine, a major regulator of allergic disease. We imaged ciliary beat frequency, mucociliary transport, apical Cl(-) permeability, and airway surface liquid (ASL) height in primary human sinonasal air-liquid-interface cultures to investigate the effects of VIP and histamine. VIP stimulated an increase in ciliary beat frequency (EC50 0.5 μM; maximal increase ∼40% compared with control) and cystic fibrosis transmembrane conductance regulator (CFTR)-dependent and Na(+)K(+)2Cl(-) cotransporter-dependent fluid secretion, all requiring cAMP/PKA signaling. Histamine activated Ca(2+) signaling that increased ASL height but not ciliary beating. Low concentrations of VIP and histamine had synergistic effects on CFTR-dependent fluid secretion, revealed by increased ASL heights. An up-regulation of VIP in histamine-driven allergic rhinitis would likely enhance mucosal fluid secretion and contribute to allergic rhinorrhea. Conversely, a loss of VIP-activated secretion in patients with CF may impair mucociliary transport, contributing to increased incidences of sinonasal infections and rhinosinusitis.

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“…Local sympathetic and parasympathetic neurons innervate nasal tissue [46,47] and release a variety of neuropeptides such as substance P (SubP), vasoactive intestinal peptide (VIP), and NPY, to control cell physiological processes such as fluid secretion, ciliary beating, and cytokine release. Parasympathetic neurons containing VIP and NPY [48][49][50][51][52][53][54][55][56][57] innervate the sinonasal cavity, including near submucosal glands of the turbinates [58][59][60] and at the pedicle of polyps [61,62]. Nasal NPYergic nerves may be increased in diseases such as allergic rhinitis [63,64] or irritative toxic rhinitis [65].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y Reduces Nasal Epithelial T2R Bitter Taste Receptor–Stimulated Nitric Oxide Production

et al. 2021

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Bitter taste receptors (T2Rs) are G-protein-coupled receptors (GPCRs) expressed on the tongue but also in various locations throughout the body, including on motile cilia within the upper and lower airways. Within the nasal airway, T2Rs detect secreted bacterial ligands and initiate bactericidal nitric oxide (NO) responses, which also increase ciliary beat frequency (CBF) and mucociliary clearance of pathogens. Various neuropeptides, including neuropeptide tyrosine (neuropeptide Y or NPY), control physiological processes in the airway including cytokine release, fluid secretion, and ciliary beating. NPY levels and/or density of NPYergic neurons may be increased in some sinonasal diseases. We hypothesized that NPY modulates cilia-localized T2R responses in nasal epithelia. Using primary sinonasal epithelial cells cultured at air–liquid interface (ALI), we demonstrate that NPY reduces CBF through NPY2R activation of protein kinase C (PKC) and attenuates responses to T2R14 agonist apigenin. We find that NPY does not alter T2R-induced calcium elevation but does reduce T2R-stimulated NO production via a PKC-dependent process. This study extends our understanding of how T2R responses are modulated within the inflammatory environment of sinonasal diseases, which may improve our ability to effectively treat these disorders.

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Neuropeptide immunofluorescence in human nasal mucosa: assessment of the technique for vasoactive intestinal peptide (VIP)

Cited by 7 publications

References 23 publications

Sinonasal Solitary Chemosensory Cells “Taste” the Upper Respiratory Environment to Regulate Innate Immunity

Sinonasal Solitary Chemosensory Cells “Taste” the Upper Respiratory Environment to Regulate Innate Immunity

Vasoactive intestinal peptide regulates sinonasal mucociliary clearance and synergizes with histamine in stimulating sinonasal fluid secretion

Neuropeptide Y Reduces Nasal Epithelial T2R Bitter Taste Receptor–Stimulated Nitric Oxide Production

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