YKL-40 is correlated with FEV1 and the asthma control test (ACT) in asthmatic patients: influence of treatment

Abstract

BackgroundYKL-40 is also called chitinase-3-like-1 (CHI3L1) protein and may be a marker for asthma. The aims of the present study were to investigate whether serum YKL-40 levels are stable or decreased in patients with asthma after appropriate treatment and to evaluate the correlation of YKL-40 levels with lung function and asthma control test (ACT) results.MethodsA total of 103 asthmatic patients (mean age 33.1 ± 0.9 years) with diagnosed asthma were enrolled in our study. All patients underwent a detailed clinical examination and completed the ACT questionnaire, serum YKL-40 measurement, and spirometry before (visit 1) and 8 weeks after initiation of treatment (visit 2).ResultsAt the follow-up, the median serum YKL-40 level was significantly decreased compared to the levels at visit 1 (75.2 [55.8-86.8] ng/ml versus 54.5 [46.4-58.4] ng/ml, p < 0.001). The serum YKL-40 level was negatively correlated with %FEV1 (r = -0.37, p < 0.001) and ACT score (r = -0.26, p = 0.007) at visit 1. The change in serum YKL-40 levels between the visits was significantly correlated with changes in FEV1 (r = -0.28, p = 0.006) and ACT score (r = -0.22, p = 0.037). Patients with elevated YKL-40 levels had significantly greater corticosteroid use than patients with lower levels.ConclusionsYKL-40 was reduced in the serum of asthmatic patients after appropriate treatment, and the levels correlated with improvements in %FEV1 and ACT. High levels of serum YKL-40 may be refractory to current asthma treatments.Trial registrationChiCTR-OCC-13003316Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2466-15-1) contains supplementary material, which is available to authorized users.

Increased YKL-40 and Chitotriosidase in Asthma and Chronic Obstructive Pulmonary Disease

“…It should be noted, however, that subjects in the BIOAIR study used inhaled corticosteroids. That could potentially have affected basal chitinase levels, as Lai and colleagues recently showed that serum YKL-40 was reduced following 8 weeks of inhaled corticosteroid treatment (49). Nevertheless, as we and others have shown, patients taking the highest doses of ICS are also those with the highest levels of YKL-40, suggesting that YKL-40 release is relatively refractory to steroid treatment (7,49).…”

“…That could potentially have affected basal chitinase levels, as Lai and colleagues recently showed that serum YKL-40 was reduced following 8 weeks of inhaled corticosteroid treatment (49). Nevertheless, as we and others have shown, patients taking the highest doses of ICS are also those with the highest levels of YKL-40, suggesting that YKL-40 release is relatively refractory to steroid treatment (7,49). One may speculate that the reason why chitinase levels are highest in patients with the most severe disease and taking the highest levels of corticosteroids is that corticosteroids are able to alternatively activate macrophages, a cell type known to release mediators involved in tissue repair (50).…”

Human amnion epithelial cells modulate the inflammatory response to ventilation in preterm lambs

“…Plasma cytokines were measured by enzyme-linked immunosorbent assay (ELISA), as detailed elsewhere [27, 28]. Briefly, 96-well flat-bottom plates (Nunc) were coated with antibody specific for IL-6 (mouse anti-ovine IL-6; 4B6, Epitope Technologies), IL-10 (mouse anti-bovine IL-10; CC318, Serotec) and TNF (mouse anti-ovine TNF; in-house) and incubated with plasma (diluted 1:1 in PBS/1% BSA/0.05% Tween 20) for 1 h at room temperature.…”

Genetic and epigenetic regulation of YKL-40 in childhood

“…1 In adults YKL-40 levels are increased in the blood and lungs of patients with asthma [2][3][4] and correlate with lung function deficits, disease severity and persistence. [2][3][4][5][6][7][8][9][10] However, to date, findings on YKL-40 and asthma in childhood have been conflicting. [11][12][13] The mechanisms linking YKL-40 with asthma remain to be determined, although in vitro and animal studies support its role in T H 2 adaptive immune responses.…”