Acute stress-induced increases in exhaled nitric oxide in asthma and their association with endogenous cortisol.
BACKGROUND
psychosocial stress is known to influence the pathophysiology of asthma. Although stress has been linked to serum markers of inflammatory activity and exaggerated response to allergen challenge in asthma, few studies have examined inflammatory activity in the airways linked to psychosocial stress alone. Furthermore, although studies have demonstrated lower levels or reactivity of endogenous cortisol in asthma, the association with airway inflammatory activity in stress remains unexplored.


OBJECTIVE
we therefore studied airway inflammation and cortisol response to a standardized laboratory task inducing acute psychosocial stress.


METHODS
airway inflammation by the fraction of exhaled nitric oxide (FeNO) and saliva cortisol were sampled before and up to 45 minutes after experimental challenge with the Trier Social Stress Test in 20 adult patients with asthma and 19 healthy control subjects. Respiratory inductive plethysmography was used to control for changes in ventilatory activity that impact FeNO levels.


RESULTS
FeNO levels were generally higher in patients with asthma than healthy control subjects and salivary cortisol levels were lower. Increases in cortisol levels were observed after the stress protocol in both groups (P < 0.001). FeNO levels at the time of peak cortisol increase after stress were significantly higher than before stress in both groups (P < 0.05). FeNO increases were independent of changes in ventilation. In patients with asthma, higher cortisol levels and stronger increases in cortisol after stress were significantly associated with smaller increases in FeNO (P < 0.05).


CONCLUSIONS
acute psychosocial stress alone increases airway inflammatory markers and this increase is attenuated by stronger stress-related activity of the hypothalamic-pituitary-adrenal axis in asthma.
Ritz
Thomas
T
Department of Psychology, Southern Methodist University, P.O. Box 750442, Dallas, TX 75275-0442, USA. tritz@smu.edu
Ayala
Erica S
ES
Trueba
Ana F
AF
Vance
Charles D
CD
Auchus
Richard J
RJ
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000378:metabolism* / Q000503:physiopathology; D001944:Breath Tests; D045853:Exhalation; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000032:analysis*; D011863:Radioimmunoassay; D012463:Saliva / Q000378:metabolism*; D012720:Severity of Illness Index; D013315:Stress, Psychological / Q000378:metabolism*; D055815:Young Adult
D009569:Nitric Oxide; D006854:Hydrocortisone