Clinical Trials Logo

Clinical Trial Summary

In severe bronchial asthma the mechanism of inflammation and bronchospasm is complex and still not clarified. The smooth muscle cells play an important role from the mechanical point of view, as a culmination of neurogenic stimuli and inflammatory cytokines that determine as final effect the bronchospasm and over time a hypertrophy of the muscular coat. There are some other hypothesis that the smooth muscle cells may play a role as central regulator of chemical mediators that cause bronchospasm and inflammation, although there are currently no firm conclusions 2 According to other studies3,the nerve receptors TRANSIENT RECEPTOR POTENTIAL VANILLOID TYPE 1 have a great importance in the complex mechanism of airway inflammation too. (There are at least 4)

These receptors would intervene according to the following mechanism:

1. Irritants on the bronchial mucosa stimulate the TRANSIENT RECEPTOR POTENTIAL VANILLOID TYPE 1 present on afferent endings of sensory fibers, unmyelinated C (chemiosensitive neurons)

2. On the same afferent axon acting factors with the activation effect (lowering the activation threshold, increase the expression, promote the translocation of TRPV1 receptor on the membrane). Among these factors the neurotrophins of which the most important NERVE GROWTH FACTOR (NGF)

3. The activation of TRPV1 (through release of Ca2 + +) determines two efferent responses:

1. CENTRALLY-MEDIATED

2. LOCAL AXON Reflex

Investigators hypothesized that BT may have a strong influence on the destruction of nerve receptors TRPV1 and unmyelinated nerve fibers located in the mucosa going to stop reflections both central and local authorities responsible for the activation of bronchospasm. In support of this hypothesis, there are some anatomical studies4, which show that these receptors are more numerous at the level of main bronchi which are the main target of BT. Please note in this context that it is already known that in thermoablations commonly used in cardiology it is used a radio frequency with development of heat controlled to 65 °, as in the BT, able to interrupt the circuit nervous responsible for the activation of the circuit causing the abnormal 'arrhythmia.


Clinical Trial Description

The mechanism of action the bronchial thermoplasty exerts the positive action demonstrated by the studies through is not yet well understood yet. The only action on the denaturation and destruction of the smooth muscle layer of the bronchi at intermediate and high caliber perhaps not fully explain its action, taking into account that most of the smooth muscle loading of the small airways is minimally altered by the procedure. From the premises outlined in the section on the mechanism of inflammation we hypothesized that BT may have a strong influence on the destruction of nerve receptors TRPV1 and unmyelinated nerve fibers located in the mucosa going to stop reflections both central and local authorities responsible for the activation of bronchospasm. In support of this hypothesis, there are some anatomical studies4, which show that these receptors are more numerous at the level of main bronchi which are the main target of BT. Please note in this context that it is already known that in thermoablations commonly used in cardiology it is used a radio frequency with development of heat controlled to 65 °, as in the BT, able to interrupt the circuit nervous responsible for the activation of the circuit causing the abnormal 'arrhythmia. ;


Study Design

Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Basic Science


Related Conditions & MeSH terms


NCT number NCT01839591
Study type Interventional
Source Arcispedale Santa Maria Nuova-IRCCS
Contact Nicola Facciolongo NF Facciolongo, M D
Phone 0522-295956
Email nicola.facciolongo@asmn.re.it
Status Recruiting
Phase N/A
Start date March 2013
Completion date December 2015

See also
  Status Clinical Trial Phase
Terminated NCT01197482 - Inhaled Steroids and Control of Severe Asthma
Withdrawn NCT02952066 - Expressions of TRPV1 in Airway of Asthmatics N/A
Completed NCT02559791 - Anti-Interleukin-5 (IL5) Monoclonal Antibody (MAb) in Prednisone-dependent Eosinophilic Asthma Phase 2/Phase 3
Recruiting NCT03617718 - Project 2 Airway Potential Hydrogen (pH) in Asthma Phase 1/Phase 2
Withdrawn NCT00954850 - A National Program for Severe Asthma: The Canadian Severe Asthma Network N/A
Completed NCT01748175 - Implications and Stability of Clinical and Molecular Phenotypes of Severe Asthma
Withdrawn NCT01745809 - Bronchoscopy Study for Severe Asthma N/A
Completed NCT02717689 - A Pragmatic Trial of Corticosteroid Optimisation in Severe Asthma N/A
Completed NCT01750411 - Severe Asthma Research Program - Wake Forest University
Completed NCT01862289 - Prevalence of Hyperventilation Syndrome in Difficult Asthma N/A
Completed NCT02659618 - Identification of Serum Biomarkers for CD15+ Hypodense Neutrophils in Severe Asthma
Withdrawn NCT00689806 - Evaluation of Lovastatin in Severe Persistent Asthma Phase 1/Phase 2