The role of neurotrophins in bronchial asthma: contribution of the pan-neurotrophin receptor p75

Prog Brain Res. 2004;146:325-33. doi: 10.1016/s0079-6123(03)46020-2.


Allergic bronchial asthma is characterized by chronic inflammation of the airways, development of airway hyperreactivity and recurrent reversible airway obstruction. Target and effector cells responsible for airway hyperresponsiveness and airway obstruction include sensory and motor neurons as well as epithelial and smooth muscle cells. Although it is well established that the inflammatory process is controlled by T-helper-2 (Th2) cells, the mechanisms by which immune cells interact with neurons, epithelial cells or smooth muscle cells still remain uncertain. Due to growing evidence for extensive communication between neurons and immune cells, the mechanisms of this neuroimmune crosstalk in lung and airways of asthmatic patients are becoming the focus of asthma research. Neurotrophins represent molecules potentially responsible for regulating and controlling the crosstalk between the immune and peripheral nervous system. They are constitutively expressed by resident lung cells and produced in increasing concentrations by immune cells invading the airways under pathological conditions. Neurotrophins modify the functional activity of sensory and motor neurons, leading to enhanced and altered neuropeptide and tachykinin production. These effects are defined as neuronal plasticity. The consequences are the development of neurogenic inflammation.

Publication types

  • Review

MeSH terms

  • Animals
  • Asthma / etiology
  • Asthma / metabolism*
  • Bronchial Hyperreactivity
  • Humans
  • Mice
  • Mice, Knockout
  • Nerve Growth Factors / physiology*
  • Neurogenic Inflammation / etiology
  • Neurogenic Inflammation / metabolism
  • Neuronal Plasticity / drug effects
  • Ovalbumin / adverse effects
  • Ovalbumin / immunology
  • Rats
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor / deficiency
  • Receptors, Nerve Growth Factor / metabolism*
  • T-Lymphocytes, Helper-Inducer / physiology
  • Tachykinins / metabolism
  • Time Factors


  • Nerve Growth Factors
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor
  • Tachykinins
  • Ovalbumin