Vasoactive intestinal peptide in human nasal mucosa.

Baraniuk, James N.; Lundgren, Jens D; Okayama, Michiko; Mullol, Joaquim; Merida, Marco; Shelhamer, James H.; Kaliner, M. A.

doi:10.1172/jci114780

Cited by 118 publications

(64 citation statements)

References 36 publications

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“…The tissue concentrations of VIP vary by anatomic site and disease condition but can enter a range (3,20,62) that we show herein is also able to activate the HCMV MIE genes in the NT2 cell model (Fig. 1).…”

Section: Discussionmentioning

confidence: 64%

Breaking Human Cytomegalovirus Major Immediate-Early Gene Silence by Vasoactive Intestinal Peptide Stimulation of the Protein Kinase A-CREB-TORC2 Signaling Cascade in Human Pluripotent Embryonal NTera2 Cells

Yuan

Liu

et al. 2009

J Virol

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. We speculate that neurohormonal stimulation via this signaling cascade is a possible means for reversing HCMV silence in vivo.Persons with impaired cellular immunity risk tissue-invasive disease from reactivation of latent human cytomegalovirus (HCMV). HCMV reactivation in tissues or blood of immunocompetent patients suffering illness from another cause also occurs but usually goes unnoticed and is self-limiting. For instance, nearly one-third of patients who are critically ill or in septic shock have detectable findings of HCMV reactivation in their bloodstream (12,26,43,45,80). HCMV reactivation infection in intestinal tissues with preexisting inflammatory disease (e.g., inflammatory bowel disease) is also well described for immunocompetent patients (28,39,40,51). The precise triggering mechanisms that underlie HCMV reactivation are unknown.So far, only cells of myeloid lineage have been determined to fulfill criteria for cellular sites of HCMV latency in vivo. In healthy HCMV-seropositive persons, precursors of macrophages and dendritic cells, including CD34ϩ hematopoietic progenitor cells, carry latent HCMV genomes at a low frequency (75). The terminal differentiation of these cells into a macrophage-or dendritic cell-like phenotype is a prerequisite for HCMV reactivation ex vivo (67, 76). However, this reactivation appears to be a rare event, suggesting that other, as yet unidentified factors may promote HCMV reactivation. Stimulation with tumor necrosis factor alpha (TNF-␣) or gamma interferon may promote HCMV reactivation from differentiated counterparts of monocytic-dendritic cell precursors that had been infected latently in vitro or in vivo (25,66,67,76).For both HCMV and murine CMV, viral major immediateearly (MIE) gene expression is greatly restricted or shut off during viral latency, and the productive viral life cycle cannot advance without this expression (57,74,75,78). The MIE enhancer/promoter controlling expression is regulated by the coordinated actions of multiple types of cis-acting elements (57). These elements are bound by cellular transcription factors whose functions are modulated by input supplied by the cell, the virus, and the external surrounding (57). Higher-order chromatin structure contributes to this regulation. Heterochromatin components amass on the inactive MIE enhancer/promoter in viral latency, whereas the chromatin signatures of transcriptional activity predominate at the active MIE enhancer/ promoter in acute and reactivation infections (47,67). MIE enhancer/promoter silencing is also favored by innate antiviral mechanisms that partly involve the repressive actions of nuclear ND10 domain components (e.g., hDAXX, PML, ATRX, and histone deacetylase [HDAC]) (52) but does not involve CpG methylation of the MIE enhancer/promoter (29).Quiescent HCMV infection of human NTera2/D1 cells (NT2 cells) is a tractable model system for studying the regulation of HCMV MIE enhancer/promoter reactivation (37, 54). NT2 cells share many phenotypic features with pluripotent

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Section: Discussionmentioning

confidence: 64%

Breaking Human Cytomegalovirus Major Immediate-Early Gene Silence by Vasoactive Intestinal Peptide Stimulation of the Protein Kinase A-CREB-TORC2 Signaling Cascade in Human Pluripotent Embryonal NTera2 Cells

Yuan

Liu

et al. 2009

J Virol

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“…In this respect, the present study was carried out cautiously to reach the highest standards of reproducibility and stringency. The 28-amino acid peptide VIP was first isolated from small intestine and lung as a vasodilatory peptide [32] and is one of the most abundant neuropeptides found in human nasal mucosa [33,34]. Although there are no reports on the effects of nasally-administered VIP in humans, it is generally accepted that VIP plays a major role in the upper respiratory tract and influences many aspects of airway function [35] due to its role as a neuromodulator of the inhibitory nonadrenergic noncholinergic nervous system [36].…”

Section: Discussionmentioning

confidence: 99%

Aspirin-sensitive rhinitis-associated changes in upper airway innervation

Groneberg

Heppt²,

Welker³

et al. 2003

European Respiratory Journal

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Aspirin-sensitive rhinitis is the manifestation of aspirin intolerance in the upper respiratory tract. The disease represents a pseudoallergy against aspirin or related nonsteroidal anti-inflammatory drugs. As a major immunomodulatory role for airway innervation has been proposed in airway inflammatory diseases, the present study assessed changes in human nasal mucosa innervation in patients with aspirinsensitive rhinitis in comparison to a control group.Immunohistochemistry for protein gene product 9.5, tachykinins, calcitonin generelated peptide, vasoactive intestinal peptide (VIP) and neuropeptide tyrosine was performed on cryostats sections of nasal mucosa and neuropeptide containing nerves were examined independently using a score grading.In comparison to the control, the aspirin-sensitive rhinitis group had a significant increase of VIP-like immunoreactivity in mucosal nerve fibres. In contrast to constant numbers of mast cells, highly significant increases in the numbers of eosinophils were found in the group of aspirin-sensitive rhinitis patients.In summary, the present quantification of neuropeptide-immunoreactivity of mucosal nerves demonstrated differences in the human nasal mucosa innervation between nonrhinitic and aspirin-sensitive rhinitic individuals. These differences may reflect a pathophysiological role of upper airway innervation in pseudoallergic reactions. Eur Respir J 2003; 22: 986-991.

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“…The inferior nasal turbinates are rich in submucosal glands, which secrete copious amounts of fluid and mucus to humidify inspired air and trap particles and pathogens. Functional and histological studies have not revealed any significant differences between nasal submucosal glands and those found in lower airways (16,(33)(34)(35)(36)(37), and intact human nasal glands also exhibit CFTR-dependent fluid secretion in response to [cAMP] i -elevating agonists (16,37).…”

Section: Low [Vip] Potentiates Cftr-dependentmentioning

confidence: 97%