According to Healio, an analysis reveals that the protein YKL-40 may be an indicator for pro-inflammatory cells but not monitoring inhaled corticosteroids in COPD patients.

“YKL-40 is mainly expressed and secreted by [pro-inflammatory macrophages] and is not further increased by pro-inflammatory stimuli. YKL-40 release is inhibited by dexamethasone in [pro-inflammatory macrophages] in vitro, whereas long-term treatment of COPD patients with inhaled corticosteroids did not significantly change YKL-40 levels in serum and sputum,” Lisette I. Z. Kunz, MD, of the department of pulmonology at Leiden University Medical Center, Leiden, Netherlands, and colleagues wrote. “This suggests that YKL-40 is a potential marker for in vitro cultured pro-inflammatory macrophages and is not a valuable biomarker in serum and sputum of patients with COPD treated with inhaled corticosteroids.”

Kunz and colleagues cultured monocytes of healthy individuals in vitro for 7 days with either granulocyte macrophage colony-stimulating factor for pro-inflammatory cells or macrophage colony-stimulating factor for anti-inflammatory cells, and all samples were stimulated for 24 hours with tumor necrosis factor alpha (TNF?), oncostatin M or pro-inflammatory stimuli lipopolysaccharide (LPS), according to the abstract. The researchers analyzed the expression of YKL-40 in macrophages using real-time polymerase chain reaction, whereas YKL-40 expression, sputum and serum levels were analyzed by enzyme-linked immunosorbent assay.

They found significantly higher YLK-40 secreted in pro-inflammatory cells than anti-inflammatory cells, which was independent of stimulation from TNF? and LPS (P < .001), according to the abstract.

“This is an important observation, since many established M?1 markers require additional stimulation to induce expression,” Kunz and colleagues wrote.

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