期刊
CLINICAL AND EXPERIMENTAL ALLERGY
卷 35, 期 6, 页码 820-825出版社
WILEY
DOI: 10.1111/j.1365-2222.2005.02264.x
关键词
allergic airway inflammation; jugular and nodose ganglia; mouse; retrograde neuronal tracing; substance P; tachykinin
Allergic airway inflammation has been shown to induce pro-inflammatory neuropeptides such as tachykinin peptides substance P (SP) and neurokinin A (NKA) together with related peptide like calcitonin gene-related peptide (CGRP) in nodose sensory neurons innervating guinea-pig airways. The present study was designed to examine the effects of allergen sensitization and challenge on the SP/NKA expression in the jugular-nodose ganglion neurons innervating the murine airways. Using retrograde neuronal tracing technique in combination with double-labelling immunohistochemistry, the expression of SP/NKA was investigated in a murine model of allergic airway inflammation. Allergic airway inflammation was found to induce the expression of SP/NKA (13.2 +/- 1.43% vs. 5.8 +/- 0.37%, P < 0.01) in large-diameter (> 20 mu m) vagal sensory neurons retrograde labelled with Fast blue dye from the main stem bronchi. Based on the induction of tachykinins in airway-specific large-sized jugular-nodose ganglia neurons by allergic airway inflammation, the present study suggests that allergen sensitization and challenge may lead to de novo induction of tachykinins in neurons. This may partly contribute to the pathogenesis of airways diseases such as allergic airway inflammation.
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