April 29, 2016
1 min read
Save

Increased YKL-40 levels linked to acute exacerbation of COPD

You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

Patients in this study with acute exacerbations of chronic obstructive pulmonary disease had elevated YKL-40 levels, indicating the glycoprotein may have a pathogenic role in the disease, according to recent research.

“The current findings demonstrate that elevated YKL-40 levels are associated with acute exacerbations and airway remodeling in patients with [chronic obstructive pulmonary disease] COPD,” Tianwen Lai, from the department of respiratory and critical care medicine, Affiliated Hospital, and institute of respiratory diseases at Guangdong Medical College in Zhanjiang, China, and colleagues wrote in their study. “Moreover, the in vitro data show that YKL-40 may promote airway remodeling in COPD by acting on human lung fibroblasts.”

Lai and colleagues evaluated the YKL-40 levels of 37 patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) and 44 patients with stable COPD and matched them against 47 control patients, according to the abstract. The researchers analyzed the effects of YKL-40 on primary human lung fibroblast collagen synthesis, as well as YKL-40 expression and airway remodeling.

They found serum YKL-40 levels were elevated at onset, with mean 78.6 ng/ml in the AECOPD group (interquartile range = 52.3 ng/ml-122.2 ng/ml) compared with 46.7 ng/ml in the stable COPD (interquartile range = 31.2 ng/ml-75.5 ng/ml) group (P = 0.0005), according to the abstract. The cut-off between AECOPD patients and stable COPD patients was 64.7 ng/ml, with an area under the curve (AUC) of 0.71 (95% CI, 0.596-0.823).

The researchers noted that factors such as airflow obstruction, collagen deposition and C-reactive protein were correlated with YKL-40 expression, according to the abstract.

“Stimulation of human lung fibroblast cells with YKL-40 resulted in a transient phosphorylation of ERK and p38. In addition, YKL-40 activated ERK and p38 phosphorylation in a dose-dependent manner,” Lai and colleagues wrote. “Overall, the current data may provide insight into the underlying pathogenesis of COPD, in which YKL-40 has an important pathogenic role.” – by Jeff Craven

Disclosure: The researchers report no relevant financial disclosures.