Aspirin-sensitive rhinitis-associated changes in upper airway innervation

Groneberg, David A.; Heppt, Werner J.; Welker, Pia; Peiser, Christian; Dinh, Q. Thai; Cryer, Annette; Zweng, Martina; Witt, Christian; Fischer, Axel

doi:10.1183/09031936.03.00086002

Cited by 25 publications

(22 citation statements)

References 38 publications

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“…The disease is a pseudoallergy against aspirin and related nonsteroidal anti-inflammatory drugs. Immunohistochemical analysis demonstrated that aspirin-sensitive rhinitis patients also had a significant increase in VIP-immunoreactive nerve fibers (80). These changes observed for the different forms of chronic upper airway inflammation may be partly regulated via neurotrophins.…”

Section: Human Respiratory Sensory Innervationmentioning

confidence: 85%

“…To assess if alterations in neuronal subpopulations are disease-specific or an epiphenomenon of the inflammation, different subtypes of chronic upper airway diseases including hyperreflectoric rhinitis (36), aspirin-sensitive rhinitis (80) and toxic rhinitis (62) have been examined. Hyperreflectoric rhinitis is a chronic upper airway inflammatory disease related to a nonspecific hyperreactivity.…”

Section: Human Respiratory Sensory Innervationmentioning

confidence: 99%

“…Next to toxic rhinitis and hyperreflectoric rhinitis, aspirin-sensitive rhinitis was investigated which represents the manifestation of aspirin intolerance in the upper airways (80). The disease is a pseudoallergy against aspirin and related nonsteroidal anti-inflammatory drugs.…”

Section: Human Respiratory Sensory Innervationmentioning

confidence: 99%

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Neurogenic mechanisms in bronchial inflammatory diseases

Groneberg

Quarcoo

Frossard

et al. 2004

Allergy

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153

103

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Neurogenic inflammation encompasses the release of neuropeptides from airway nerves leading to inflammatory effects. This neurogenic inflammatory response of the airways can be initiated by exogenous irritants such as cigarette smoke or gases and is characterized by a bi‐directional linkage between airway nerves and airway inflammation. The event of neurogenic inflammation may participate in the development and progression of chronic inflammatory airway diseases such as allergic asthma or chronic obstructive pulmonary disease (COPD). The molecular mechanisms underlying neurogenic inflammation are orchestrated by a large number of neuropeptides including tachykinins such as substance P and neurokinin A, or calcitonin gene‐related peptide. Also, other biologically active peptides such as neuropeptide tyrosine, vasoactive intestinal polypeptide or endogenous opioids may modulate the inflammatory response and recently, novel tachykinins such as virokinin and hemokinins were identified. Whereas the different aspects of neurogenic inflammation have been studied in detail in laboratory animal models, only little is known about the role of airway neurogenic inflammation in human diseases. However, different functional properties of airway nerves may be used as targets for future therapeutic strategies and recent clinical data indicates that novel dual receptor antagonists may be relevant new drugs for bronchial asthma or COPD.

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Section: Human Respiratory Sensory Innervationmentioning

confidence: 85%

Section: Human Respiratory Sensory Innervationmentioning

confidence: 99%

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Neurogenic mechanisms in bronchial inflammatory diseases

Groneberg

Quarcoo

Frossard

et al. 2004

Allergy

Self Cite

153

103

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“…Apart from the potential role in drug therapy, the transporters also transport peptide fragments and may scavenge peptide from the oropharyngeal cavity back into the systemic circulation. In this respect, it has been shown that numerous neuropeptides are up-regulated in different states of upper airway inflammation such as toxic rhinitis [38], intermittent seasonal allergic rhinitis [39], perennial allergic rhinitis [40], aspirin-sensitive rhinitis [41] or hyperreflectoric rhinitis [42]. Also, the transporters may function as uptake system for neurotrophin or tachykinin fragments [43,44,45].…”

Section: Discussionmentioning

confidence: 99%

Expression, Localisation and Functional Implications of the Transporter Protein PEPT2 in the Upper Respiratory Tract

Quarcoo¹,

Fischer

Heppt

et al. 2008

Respiration

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Infectious diseases of the upper respiratory tract are widespread and may initiate exacerbations of chronic respiratory diseases such as bronchial asthma or chronic obstructive pulmonary disease. Nebulisation of antibiotics as a topic treatment may lead to high local drug concentrations. To provide data on drug transport, the present study analysed a specific drug transport system on the molecular and functional level. Messenger RNA of the proton-coupled transporter PEPT2 that mediates physiological transport of oligopeptides as well as peptidomimetics like β-lactams and aminolevulinic acid was discovered in rat nasal mucosa by RT-PCR. Real-time PCR studies indicated a lower expression level than control kidney samples. PEPT2 immunoreactivity was identified in nasal mucosa tissue. The protein was expressed in epithelial cells, but goblet cells did not exhibit PEPT2 expression. Functional studies with rat preparations led to uptake of a fluorophore-conjugated substrate into epithelial cells of nasal mucosa. Goblet cells did not exhibit uptake activity. The uptake was competitively inhibited by dipeptides demonstrating similar substrate specificity as reported for PEPT2. Together, these data suggest that PEPT2 is likely to play an important role in mucosal peptide metabolism and may represent a novel target for therapeutic efforts in upper airway diseases.

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“…To examine whether changes in neuronal populations are disease-specific or an epiphenomenon of inflammation the different rhinitis forms have been examined for example hyperreflectoric rhinitis [12], aspirin-sensitive rhinitis [66] and toxic rhinitis [67].…”

Section: Role In Airway Inflammationmentioning

confidence: 99%

Tachykinins in the Respiratory Tract

Groneberg

Harrison²,

Dinh³

et al. 2006

CDT

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Tachykinins as substance P and neurokinin A belong to a family of peptides, which are released from airway nerves after noxious stimulation. They influence numerous respiratory functions under both normal and pathological conditions including the regulation of airway smooth muscle tone, vascular tone, mucus secretion and immune functions. For the most part the synthesis/release of tachykinins is associated with neuronal cells; nevertheless, inflammatory and immune cells can synthesize and release tachykinins under certain physiological conditions. Moreover, this second cellular source of tachykinins may play an important role in inflammatory airway diseases such as bronchial asthma or chronic obstructive pulmonary disease (COPD). Dual tachykinin (NK1 and NK2) receptor antagonists demonstrate a significant bronchoprotection and a possible future role in the development of novel therapeutic approaches. In addition, NK3 receptors could also possess a bronchoprotective action, however, their presence in the human respiratory tract still needs to be confirmed. The family of tachykinins has recently been extended by the discovery of a third tachykinin gene that encodes the previously unknown NK1 receptor selective tachykinins hemokinin 1, endokinin A and B. Together with other novel tachykinin peptides such as C14TKL-1 and virokinin further research is required to define their respiratory biological role in health and disease.

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Aspirin-sensitive rhinitis-associated changes in upper airway innervation

Cited by 25 publications

References 38 publications

Neurogenic mechanisms in bronchial inflammatory diseases

Neurogenic mechanisms in bronchial inflammatory diseases

Expression, Localisation and Functional Implications of the Transporter Protein PEPT2 in the Upper Respiratory Tract

Tachykinins in the Respiratory Tract

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