Asthma is a complex disease with a variable course. Efforts to
identify biomarkers to predict asthma severity, the course of
disease and response to treatment have not been very successful
so far. Biomarker research has expanded greatly with the
advancement of molecular research techniques. An ideal
biomarker should be suitable to identify the disease as well the
specific endotype/phenotype, useful in the monitoring of the
disease and to determine the prognosis, easily to obtain with
minimum discomfort or risk to the patient. An ideal biomarker
should be suitable to identify the disease as well the specific
endotype/phenotype, useful in the monitoring of the disease and
to determine the prognosis, easily to obtain with minimum
discomfort or risk to the patient - exhaled breath analysis, blood
cells and serum biomarkers, sputum cells and mediators and urine
metabolites could be potential biomarkers of asthma bronchiale.
Unfortunately, at the moment, an ideal biomarker doesn’t exist and
the overlap between the biomarkers is a reality. Using panels of
biomarkers could improve probably the identification of asthma
endotypes in the era of precision medicine.
New knowledge about the neural aspects of cough has revealed
a complex network of pathways that initiate cough. The effect of
inflammation on cough neural processing occurs at multiple
peripheral and central sites within the nervous system. Evidence
exists that direct or indirect neuroimmune interaction induces
a complex response, which can be altered by mediators released
by the sensory or parasympathetic neurons and vice versa. The
aim of this study was to clarify changes of cough reflex sensitivity
– the activity of airway afferent nerve endings - in asthmatic
children. 25 children with asthma and 15 controls were submitted
to cough reflex sensitivity measurement - capsaicin aerosol in
doubling concentrations (from 0.61 to 1250 µmol/l) was inhaled
by a single breath method. Concentrations of capsaicin causing
two (C2) and five coughs (C5) were reported. Asthmatic children'
(11 boys and 14 girls, mean age 9 ± 1 yrs) cough reflex sensitivity
(geometric mean, with the 95 % CI) for C2 was 4.25 (2.25-8.03)
µmol/l vs. control C2 (6 boys and 9 girls, mean age 8 ± 1 yrs) was
10.61 (5.28-21.32) µmol/l (p=0.024). Asthmatic children' C5 was
100.27 (49.30-203.93) µmol/l vs. control C5 56.53 (19.69-162.35)
µmol/l (p=0.348). There was a statistically significant decrease of
C2 (cough threshold) in the asthmatic patients relative to controls
(p-value for the two-sample t-test of log(C2) for the one-sided
alternative, p-value = 0.024). The 95 % confidence interval for the
difference of the mean C2 in asthma vs. control, [1.004, 6.207].
For C5, the difference was not statistically significant (p-value =
0.348). There was a statistically significant decrease of cough
reflex sensitivity (the activity of airway afferent nerve endings) -
C2 value in the asthmatic children relative to controls.
Cough is one of the most important defensive reflexes. However,
extensive non- productive cough is a harmful mechanism leading
to the damage of human airways. Cough is initiated by activation
of vagal afferents in the airways. The site of their convergence is
particularly the nucleus of the solitary tract (nTS). The secondorder neurons terminate in the pons, medulla and spinal cord and
there is also the cortical and subcortical control of coughing. Upper
airway cough syndrome (UACS) – previously postnasal drip
syndrome - is one of the most common causes of chronic cough
together with asthma and gastroesophageal reflux. The main
mechanisms leading to cough in patients with nasal and sinus
diseases are postnasal drip, direct irritation of nasal mucosa,
inflammation in the lower airways, upper airway inflammation and
the cough reflex sensitization. The cough demonstrated by UACS
patients is probably due to hypersensitivity of the upper airways
sensory nerve or lower airways sensory nerve, or a combination of
both. Further studies are needed to clarify this mechanism.