Volume 34, Issue 12 pp. 1934-1941

Expression of tyrosine hydroxylase and neuropeptide tyrosine in mouse sympathetic airway-specific neurons under normal situation and allergic airway inflammation

Q. T. Dinh

Q. T. Dinh

Department of Internal Medicine,

Clinical Research Unit of Allergy and

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D. A. Groneberg

D. A. Groneberg

Clinical Research Unit of Allergy and

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C. Witt

C. Witt

Department of Pneumology, Charité School of Medicine, Humboldt University, Berlin, Germany

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C. Peiser

C. Peiser

Clinical Research Unit of Allergy and

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L. B. Cifuentes

L. B. Cifuentes

Clinical Research Unit of Allergy and

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N. Frossard

N. Frossard

INSERM U 425, Pulmonary Neuroimmunopharmacology, University of Strasbourg, Illkirch, Strasbourg, France

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B. F. Klapp

B. F. Klapp

Department of Internal Medicine,

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A. Fischer

A. Fischer

Clinical Research Unit of Allergy and

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First published: 15 November 2004
Citations: 7
Q. Thai Dinh, Department of Internal Medicine and Clinical Research Unit of Allergy, Charite, Virchow Campus, Ostring 3, R. 3.0066, Augustenburger Platz 1, D-13353 Berlin, Germany.
E-mail: [email protected]

Summary

Background The traditional neurotransmitter catecholamine and the neuropeptide tyrosine in sympathetic airway nerves have been proposed to be involved in the pathogenesis of airway diseases.

Objective The aim of the present study was to investigate the effect of allergic airway inflammation on the expression of catecholamine enzyme tyrosine hydroxylase (TH), neuropeptide tyrosine (NPY) and tachykinins in mouse sympathetic airway ganglia.

Methods Using neuronal tracing in combination with immunohistochemistry, the present study was designed to characterize TH, NPY and tachykinin profiles of superior cervical (SCG) and stellate ganglia after allergen challenge.

Results The vast majority of fast blue-labelled SCG neurons (allergen: 97.5±1.22% (mean±SEM) vs. controls: 94.5±1.48%, P=0.18) and stellate neurons (allergen: 95.3±1.01% vs. controls: 93.6±1.33%, P=0.34) were immunoreactive for TH. Of the TH immunoreactive and fast blue-labelled SCG neurons, 52.0±1.01% allergen vs. 51.2±3.58% controls (P=0.83) and stellate neurons, 57.3%±0.97 allergen vs. 56.4±1.65% controls (P=0.64) were positive for TH only but not NPY, whereas 45.3±1.05% allergen vs. 43.3±1.18% controls (P=0.47) of fast blue-labelled SCG neurons and 37.9±0.86% allergen vs. 37.1±1.24% controls (P=0.62) of fast blue-labelled stellate neurons were immunoreactive for both TH and NPY immunoreactivities. There was a trend of an increase, but not significant one, in the percentage of TH-/NPY-immunoreactive and fast blue-labelled neurons in allergen-treated animals in comparison with the controls. Tachykinins, however, were not expressed by sympathetic neurons and were also not induced in sympathetic neurons after allergen challenge.

Conclusion The present study indicates that allergic airway inflammation does not alter the expression of noradrenalin and NPY in sympathetic ganglia and also shows that sympathetic neurons do not respond to allergic airway inflammation with tachykinins induction. However, a participation of catecholamine and NPY in the pathogenesis of allergic airway inflammation cannot be excluded in the present study as a higher neurotransmitter output per neuron following allergen challenge could be possible.

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