Dinh Q T, Mingomataj E, Quarcoo D, Groneberg D A, Witt C, Klapp B F, Braun A, Fischer A
Department of Internal Medicine, Charité School of Medicine, Humboldt and Freie University Berlin, Berlin, Germany.
Clin Exp Allergy. 2005 Jun;35(6):820-5. doi: 10.1111/j.1365-2222.2005.02264.x.
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 microm) 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.
变应性气道炎症已被证明可诱导豚鼠气道的结状感觉神经元中促炎神经肽的产生，如速激肽P物质（SP）和神经激肽A（NKA），以及相关肽如降钙素基因相关肽（CGRP）。
本研究旨在检测变应原致敏和激发对支配小鼠气道的颈-结状神经节神经元中SP/NKA表达的影响。
采用逆行神经元追踪技术结合双标记免疫组织化学方法，在变应性气道炎症小鼠模型中研究SP/NKA的表达。
在经主支气管Fast blue染料逆行标记的大直径（>20μm）迷走感觉神经元中，发现变应性气道炎症可诱导SP/NKA的表达（13.2±1.43%对5.8±0.37%，P<0.01）。
基于变应性气道炎症可诱导气道特异性大尺寸颈-结状神经节神经元中速激肽的产生，本研究提示变应原致敏和激发可能导致神经元中速激肽的从头诱导。这可能部分促成气道疾病如变应性气道炎症的发病机制。
