Allergic airway inflammation induces tachykinin peptides expression in vagal sensory neurons innervating mouse airways

被引:34
作者
Dinh, QT
Mingomataj, E
Quarcoo, D
Groneberg, DA
Witt, C
Klapp, BF
Braun, A
Fischer, A
机构
[1] Humboldt Univ, Dept Internal Med, D-13353 Berlin, Germany
[2] Free Univ Berlin, Clin Res Unit Allergy, Berlin, Germany
[3] Free Univ Berlin, Dept Pediat Pneumol & Immunol, Berlin, Germany
[4] Free Univ Berlin, Dept Pneumol, Charite Sch Med, Berlin, Germany
[5] Fraunhofer Inst Toxicol & Expt Med, Dept Immunol & Allergol, Hannover, Germany
关键词
allergic airway inflammation; jugular and nodose ganglia; mouse; retrograde neuronal tracing; substance P; tachykinin;
D O I
10.1111/j.1365-2222.2005.02264.x
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:820 / 825
页数:6
相关论文
共 36 条
[1]   Substance P antagonists: novel agents in the treatment of depression [J].
Argyropoulos, SV ;
Nutt, DJ .
EXPERT OPINION ON INVESTIGATIONAL DRUGS, 2000, 9 (08) :1871-1875
[2]   MODULATION OF NEUROTRANSMISSION IN AIRWAYS [J].
BARNES, PJ .
PHYSIOLOGICAL REVIEWS, 1992, 72 (03) :699-729
[3]  
Barnes PJ, 1998, PHARMACOL REV, V50, P515
[4]  
BARNES PJ, 1986, LANCET, V1, P242
[5]   Adjuvant-induced joint inflammation causes very rapid transcription of β-preprotachykinin and α-CGRP genes in innervating sensory ganglia [J].
Bulling, DGS ;
Kelly, D ;
Bond, S ;
McQueen, DS ;
Seckl, JR .
JOURNAL OF NEUROCHEMISTRY, 2001, 77 (02) :372-382
[6]   Pharmacology of vagal afferent nerve activity in guinea pig airways [J].
Carr, MJ ;
Undem, BJ .
PULMONARY PHARMACOLOGY & THERAPEUTICS, 2003, 16 (01) :45-52
[7]   The capsaicin receptor: a heat-activated ion channel in the pain pathway [J].
Caterina, MJ ;
Schumacher, MA ;
Tominaga, M ;
Rosen, TA ;
Levine, JD ;
Julius, D .
NATURE, 1997, 389 (6653) :816-824
[8]   Nerve growth factor induces a neurokinin-1 receptor-mediated airway hyperresponsiveness in guinea pigs [J].
de Vries, A ;
Dessing, MC ;
Engels, F ;
Henricks, PAJ ;
Nijkamp, FP .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 159 (05) :1541-1544
[9]   Expression of substance P and vanilloid receptor (VR1) in trigeminal sensory neurons projecting to the mouse nasal mucosa [J].
Dinh, QT ;
Groneberg, DA ;
Mingomataj, E ;
Peiser, C ;
Heppt, W ;
Dinh, S ;
Arck, PC ;
Klapp, BF ;
Fischer, A .
NEUROPEPTIDES, 2003, 37 (04) :245-250
[10]  
DINH QT, 2004, NERVE GROWTH FACTOR