Objective: To investigate the role of anaphylatoxin C5a in the pathogenesis of chronic obstructive pulmonary disease (COPD).
Methods: A total of 64 elderly patients with COPD (31 acute exacerbation of COPD, 34 stable COPD) and 15 healthy subjects were recruited into the study. Lung function, the levels of serum C5a and high sensitivity CRP (hs-CRP), and the levels of C5a, IL-8 and cell differentials in induced sputum were determined. For nonnormally distributed variables, differences between two groups were analysed using a Mann-Whitney u test, and comparison of three groups was performed using analysis of Kruskal-Wallis test. For normally distributed variables, differences between two groups were analyzed using unpaired t test, and comparison of three groups was performed using analysis of one-way ANOVA. Comparisons of the groups were performed using Chi-squared test for enumeration data. The association between variables was assessed by Spearman rank-order method.
Results: The levels of serum C5a in acute exacerbation of COPD [215 (109 - 376) microg/L] were higher than those in stable COPD [91 (53 - 365) microg/L, z = -2.123, P < 0.05], and were positively correlated with the level of serum hs-CRP (r = 0.574, P < 0.05), and negatively correlated with FEV1% predicted (r = -0.562, P < 0.05). The levels of C5a in induced sputum in acute exacerbation of COPD [1.8 (1.0 - 3.2) microg/L] were significantly higher than those in stable COPD [0.9 (0.2 - 2.4) microg/L, z = - 2.079, P < 0.05] and were positively correlated with the level of IL-8 in induced sputum (r = 0.518, P < 0.05). The levels of C5a in induced sputum in stable COPD were significantly higher than those in healthy subjects [0.3 (0.1 - 0.7) microg/L, z = -2.044, P < 0.05]. The level of C5a in induced sputum was positively correlated with the number of total cells count (r = 0.441, P < 0.05), the percentage of neutrophils (r = 0.439, P < 0.05) and macrophages (r = 0.449, P < 0.05) in acute exacerbation of COPD.
Conclusion: Anaphylatoxin (C5a) may be involved in the pathogenesis of COPD.