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Pan-neurotrophin receptor p75 contributes to neuronal hyperreactivity and airway inflammation in a murine model of experimental asthma

: Kerzel, S.; Päth, G.; Nockher, W.A.; Quarcoo, D.; Raap, U.; Groneberg, D.A.; Dinh, Q.T.; Fischer, A.; Braun, A.; Renz, H.


American journal of respiratory cell and molecular biology 28 (2003), pp.170-178
ISSN: 1044-1549
ISSN: 1535-4989
Journal Article
Fraunhofer ITEM ()
airway hyperresponsiveness; fetal calf serum; ovalbumin; phosphate-buffered saline; substance P; time of break; tris-buffered saline; tyrosin kinase receptor; interleukin; immunoglobulins; nerve growth factor; tyrosine; interferon

Bronchial asthma represents a severe chronic inflammatory disease with increasing prevalence. The pathogenesis is characterized by complex neuroimmune dysregulation. Although the immunopathogenesis of the disease has been extensively studied, the nature of neuronal dysfunction still remains poorly understood. Recent data indicate that neurotrophins contribute to airway inflammation, broncho-obstruction and airway hyperresponsiveness. Using an established murine model of allergic bronchial asthma, the contribution of the pan-neurotrophin receptor p75(NTR) was defined. This receptor is expressed both in normal and asthmatic lungs and airways. Analysis of p75(NTR-/-) mice, as well as in vivo blocking of p75(NTR), revealed that airway inflammation is to a large extent dependent upon functional receptor expression. Furthermore, neuronal hyperreactivity depends entirely on this receptor. Based on these data, a novel molecular pathway in the neuroimmune pathogenesis of bronchial asthma could be defined.