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YKL-40 expression possible marker for pro-inflammatory cells

An analysis of cultured monocytes from healthy individuals has revealed that the soluble chitinase-like-protein YKL-40 may be an indicator for pro-inflammatory cells, but not for monitoring inhaled corticosteroids in patients with chronic obstructive pulmonary disease.

“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 (TNFα), 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 TNFα and LPS (P < .001), according to the abstract.

“This is an important observation, since many established MΦ1 markers require additional stimulation to induce expression,” Kunz and colleagues wrote.

Further, the researchers found “dexamethasone efficiently suppressed YKL-40 expression and secretion in [pro-inflammatory cells], but that this was mainly explained by an inhibitory effect of dexamethasone on [pro-inflammatory cells] differentiation, thus extending previous results.”

Kunz and colleagues also noted that patients with COPD had higher YKL-40 serum levels compared to sputum levels, but inhaled corticosteroid treatments did not change this result. – by Jeff Craven

Disclosure: This study was funded by Netherlands Organization for Scientific Research, Lung Foundation Netherlands, GlaxoSmithKline of The Netherlands, the University Medical Center Groningen and Leiden University Medical Center.