Die sensible Atemwegsinnervation und die Tachykinine bei Asthma und chronisch-obstruktiver Lungenerkrankung (COPD)

Abstract

The airway nerve has gained importance in the field of respiratory research as it is known to have the capacity to release numerous mediators which can cause pulmonary effects in the airways. Meanwhile, a broad range of stimuli including capsaicin, bradykinin, hyperosmolar saline, tobacco smoke, allergens, ozone, inflammatory mediators and cold dry air have been shown to activate sensory nerve fibres to release neuropeptides such as the tachykinins substance P (SP) and neurokinin A (NKA) to mediate neurogenic inflammation. SP is synthesized in cell bodies of airway neurons of the trigeminal, jugulare and nodose ganglia. Following their release, tachykinins are degraded by neutral endopeptidase (NEP) and an angiotensin-converting enzyme. Tachykinins have been proposed to play an important role in human respiratory diseases such as bronchial asthma und chronic obstructive diseases (COPD) as they have been shown to have potent effects on the tone of airway smooth muscle, airway secretions, bronchial circulation and on inflammatory and immune cells by activation of the neurokinin-1 (NK-1) and neurokinin-2 (NK-2) receptors. Recently, new tachykinins such as virokinin and hemokinin were identified and characterised. Different aspects of the neurogenic inflammation have been well studied in animal models of allergic airway inflammation, but only little is known about the role of neurogenic airway inflammation in human diseases. To address the precise role of tachykinins and airway sensory nerves in human asthma und COPD, experiments on sensory nerve sensitisation and neuro-immune interaction have to be carried out in future studies.

Mycoplasma hyopneumoniae surface-associated proteases cleave bradykinin, substance P, neurokinin A and neuropeptide Y

“…However, the ability to induce cough has since been contested 62 . Like SP, NKA induces bronchoconstriction and mucus production in the lungs as well as neurogenic inflammation 63 . Additionally, NKA is a potent attractor of T-cells 57 .…”

Inhaled corticosteroids inhibit substance P receptor expression in asthmatic rat airway smooth muscle cells

“…Neurokinins (NKs) are peptides synthesized by neural tissues that have been implicated as the mediators of neurogenic inflammation in asthma. NKs have potent effects on airway smooth muscle tone, airway secretion, bronchial circulation, and inflammatory and immune cells via the activation of the neurokinin-1 (NK-1R) and neurokinin-2 receptors (NK-2R); as such, they have been proposed to play an important role in human respiratory conditions such as bronchial asthma and chronic obstructive diseases [2]. For example, Pattersson et al demonstrated that tachykinin levels were increased in induced sputum from patients with asthma, cough, and acid reflux [3].…”

The effect of substance P on asthmatic rat airway smooth muscle cell proliferation, migration, and cytoplasmic calcium concentration in vitro

“…Tachykinins have been proposed to play an important role in human respiratory diseases such as bronchial asthma and chronic obstructive pulmonary diseases (COPD), as they have been shown to activate the neurokinin (NK)-1 and NK-2 receptors, leading to potent effects on airway smooth muscle tone and secretions, bronchial circulation, and inflammatory and immune cells [10]. Tachykinin levels were increased in induced sputum from asthmatic and cough patients with acid reflux [11].…”