Patients with acute exacerbations of COPD had elevated YKL-40 levels, which suggests glycoprotein may have a pathogenic role in the disease, according to a study. The researchers evaluated the YKL-40 levels of 37 patients with acute exacerbations of COPD (AECOPD) and 44 patients with stable COPD and matched them against 47 control patients, according to the study abstract. The research team then analyzed the effects of YKL-40 on primary human lung fibroblast collagen synthesis as well as YKL-40 expression and airway remodeling.
The study abstract notes that researchers 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), as reported by Healio. The cut-off between AECOPD patients and stable COPD patients was 64.7 ng/ml, with an area under the curve of 0.71.
“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,” write Tianwen Lao and colleagues. “Moreover, the in vitro data show that YKL-40 may promote airway remodeling in COPD by acting on human lung fibroblasts.”
The researchers noted that factors such as airflow obstruction were correlated with YKL-40 expression, as noted in the study abstract.
The researchers write, “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. Overall, the current data may provide insight into the underlying pathogenesis of COPD, in which YKL-40 has an important pathogenic role.”