[Airway inflammation and peripheral airway function in asthmatic patients with different control levels]

To observe the airway inflammation and peripheral airway function in asthmatic patients with different control levels, and to investigate whether the airway inflammation profile detected by induced sputum reflects the peripheral airway dysfunction.

The recruited asthmatic subjects (n = 66) were divided into 3 groups: asthma controlled (8 male and 13 female), asthma partly controlled (12 male and 16 female), asthma uncontrolled (6 male and 11 female). Twenty healthy subjects served as the control group (9 male and 11 female). On the 1(st) day, all the subjects were required to take asthma control test (ACT), and to receive measurement of lung function by oscillometry and spirometry as well as inflammatory cell profile of induced sputum and the concentration of eosinophil cationic protein (ECP). Exhaled nitric oxide (FE(NO)) was measured on the 2(nd) day, and oscillometry methacholine provocation was conducted for patients whose baseline FEV(1) was > or = 70% predicted. The provocation process was terminated when airway resistance was increased by twice of the basic value, or when the methacholine reached the highest concentration. Then airway resistance and lung function were examined after 3 minutes. Finally, airway resistance and lung function were measured again after the subjects had 5 consecutive deep inspirations (DI). Correlation analysis was conducted between ACT scores and inflammatory cells count, ECP concentrations of induced sputum and FE(NO) among different groups. The correlations were also made between the change of peripheral airway resistance triggered by provocation or DI and ACT scores, total eosinophil, ECP level of induced sputum, FE(NO) respectively.

The total eosinophil count and ECP level in induced sputum and FE(NO) in asthmatic patients increased with the decline of control level. Negative correlations between ACT scores and total eosinophil count as well as the ECP level were observed (r = -0.43, -0.56, P < 0.01). In the healthy control group, the percentage of increase in peripheral airway resistance (R(5)-R(20)) and central airway resistance (R(20)) did not show significant difference (F = 3.472, P > 0.05) with methacholine provocation, while the percentage of increase in R(5)-R(20) was greater than in R(20) in both controlled and partly controlled asthmatic patients with provocation (F = 18.09 and 14.14, P < 0.01), though the change of R(5)-R(20) showed no correlations with ACT scores, eosinophil count of induced sputum, ECP level and FE(NO). After DI, R(5)-R(20) decreased from (0.13 +/- 0.14) kPa x L(-1) x s(-1) to (0.08 +/- 0.09) kPa x L(-1) x s(-1) (t = 2.84, P < 0.05) in the healthy control group, while R(5)-R(20) increased from (0.24 +/- 0.15) kPa x L(-1) x s(-1) to (0.30 +/- 0.16) kPa x L(-1) x s(-1) in the controlled asthma group, from (0.31 +/- 0.18) kPa x L(-1) x s(-1) to (0.39 +/- 0.17) kPa x L(-1) x s(-1) in the partly controlled asthma group (t = 3.90 and 4.68, P < 0.01, respectively). No correlations were observed between the change of R(5)-R(20) after DI and ACT scores, total eosinophil counts, ECP level as well as FE(NO) (r = -0.07, 0.28, -0.14, 0.14, P > 0.05).

Even in asthma patients with controlled disease, eosinophilic inflammation in the airway was still present, and the eosinophilic inflammation became more severe with the decline of control level. Bronchodilatory effect caused by DI disappeared in asthmatic patients. The inflammation profile detected by induced sputum did not reflect the dysfunction of peripheral airways.