title: Pan-neurotrophin receptor p75 contributes to neuronal hyperreactivity and airway inflammation in a murine model of experimental asthma.
abstract: 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.
authors.affiliation: Department of Clinical Chemistry and Molecular Diagnostics, Philipps-University Marburg, Marburg, Germany.
authors.forename: Sebastian
authors.initials: S
authors.lastname: Kerzel
authors.forename: Günter
authors.initials: G
authors.lastname: Päth
authors.forename: Wolfgang A
authors.initials: WA
authors.lastname: Nockher
authors.forename: David
authors.initials: D
authors.lastname: Quarcoo
authors.forename: Ulrike
authors.initials: U
authors.lastname: Raap
authors.forename: David A
authors.initials: DA
authors.lastname: Groneberg
authors.forename: Q Thai
authors.initials: QT
authors.lastname: Dinh
authors.forename: Axel
authors.initials: A
authors.lastname: Fischer
authors.forename: Armin
authors.initials: A
authors.lastname: Braun
authors.forename: Harald
authors.initials: H
authors.lastname: Renz
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D007249:Inflammation / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009414:Nerve Growth Factors / Q000502:physiology; D009474:Neurons / Q000502:physiology; D010047:Ovalbumin / Q000276:immunology; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D012137:Respiratory System / Q000294:innervation; D013373:Substance P / Q000378:metabolism
chemical_list: D009414:Nerve Growth Factors; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D013373:Substance P; D010047:Ovalbumin