YKL-40 in asthmatic patients, and its correlations with exacerbation, eosinophils and immunoglobulin E

Tang, Hao; Zheng, Fang; Sun, Yinghao; Li, B; Shi, Zhenxiang; Chen, J; Zhang, T; Xiu, Qingyu

doi:10.1183/09031936.00034409

Cited by 90 publications

(78 citation statements)

References 16 publications

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“…Serum YKL-40 levels and chitotriosidase activity have not previously been examined in parallel in patients with COPD and patients with asthma. The finding of increased serum YKL-40 in patients with asthma confirms previous observations (7,8,24,25). The higher levels in patients with severe asthma than in patients with mild asthma, along with the correlation between YKL-40 and reduced lung function, strengthen the association of serum YKL-40 with disease severity (7,8).…”

Section: Discussionsupporting

confidence: 79%

“…The higher levels in patients with severe asthma than in patients with mild asthma, along with the correlation between YKL-40 and reduced lung function, strengthen the association of serum YKL-40 with disease severity (7,8). The exact biological role of YKL-40 remains unclear, but it consistently correlates with airway obstruction in studies of patients with asthma (7,8,24). YKL-40 associates with measures of airway remodeling, such as bronchial wall thickness and subepithelial Figure 2.…”

Section: Discussionmentioning

confidence: 99%

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

James

Reinius

Verhoek

et al. 2016

Am J Respir Crit Care Med

113

102

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Rationale: Serum chitinases may be novel biomarkers of airway inflammation and remodeling, but less is known about factors regulating their levels.Objectives: To examine serum chitotriosidase activity and YKL-40 levels in patients with asthma and chronic obstructive pulmonary disease (COPD) and evaluate clinically relevant factors that may affect chitinase levels, including genetic variability, corticosteroid treatment, disease exacerbations, and allergen exposure.Methods: Serum chitotriosidase (CHIT1) activity and YKL-40 (CHI3L1) levels, as well as the CHIT1 rs3831317 and CHI3L1 rs4950928 genotypes, were examined in subsets of patients with mild to moderate asthma (n = 76), severe asthma (n = 93), and COPD (n = 64) taking part in the European multicenter BIOAIR (Longitudinal Assessment of Clinical Course and Biomarkers in Severe Chronic Airway Disease) study. Blood was obtained at baseline, before and after a 2-week oral steroid intervention, up to six times during a 1-year period, and during exacerbations. Baseline chitinase levels were also measured in 72 healthy control subjects. The effect of allergen inhalation on blood and sputum YKL-40 levels was measured in two separate groups of patients with mild atopic asthma; one group underwent repeated low-dose allergen challenge (n = 15), and the other underwent high-dose allergen challenge (n = 16).Measurements and Main Results: Serum chitotriosidase and YKL-40 were significantly elevated in patients with asthma and those with COPD compared with healthy control subjects. Genotype and age strongly affected both YKL-40 and chitotriosidase activity, but associations with disease remained following adjustment for these factors. Correlations were observed with lung function but not with other biomarkers, including exhaled nitric oxide, blood eosinophils, periostin, and IgE. Generally, acute exacerbations, allergen-induced airway obstruction, and corticosteroid treatment did not affect circulating chitinase levels.Conclusions: YKL-40 and chitotriosidase are increased in asthma and more so in COPD. The data in the present study support these substances as being relatively steroid-insensitive, non-T-helper cell type 2-type biomarkers distinctly related to chronic inflammatory disease processes.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

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

James

Reinius

Verhoek

et al. 2016

Am J Respir Crit Care Med

113

102

View full text Add to dashboard Cite

show abstract

“…In asthma, increased serum levels and lung expression of YKL-40 are correlated with disease severity, airway remodeling, and decreased pulmonary function (17). Our previous study also showed that the elevated serum YKL-40 levels in asthmatics were correlated positively with total serum IgE levels and the percentage of peripheral blood eosinophils and correlated inversely with lung functions (18). Based on these findings, YKL-40 is believed to be involved in the pathogenesis of asthma and has attracted the attention of many groups during last few years.…”

mentioning

confidence: 76%

YKL-40 Induces IL-8 Expression from Bronchial Epithelium via MAPK (JNK and ERK) and NF-κB Pathways, Causing Bronchial Smooth Muscle Proliferation and Migration

Tang

Sun

Shi

et al. 2013

The Journal of Immunology

108

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Recently, the serum levels of YKL-40, a chitinase-like glycoprotein, have been shown to be significantly elevated in asthmatics and are associated with asthma severity. Although these studies raise the possibility that YKL-40 may influence asthma, the mechanisms remain unknown. This study firstly investigated the mechanisms involved in YKL-40–mediated inflammation in human bronchial epithelial cells (HBECs) and analyzed the soluble factors secreted by bronchial epithelial cells exposed to YKL-40 that were responsible for increasing proliferation and migration of primary normal human bronchial smooth muscle cells (BSMCs). YKL-40–induced inflammation was assayed in two HBECs (BEAS-2B cell line and primary HBECs). In addition, we treated BEAS-2B cells and HBECs with YKL-40 and added the conditioned culture media to BSMCs. The proliferation and migration of BSMCs were determined by premixed WST-1 cell proliferation reagent (Clontech Laboratories) and QCM chemotaxis migration assay (Millipore), respectively. Bronchial epithelial cells treated with YKL-40 resulted in a significant increase of IL-8 production, which was dependent on MAPK (JNK and ERK) and NF-κB pathways activation. YKL-40–induced IL-8 was found to further stimulate proliferation and migration of BSMCs, and the effects were inhibited after neutralizing IL-8. Through investigating the interaction of airway epithelium and smooth muscle, our findings implicate that YKL-40 may be involved in the inflammation of asthma by induction of IL-8 from epithelium, subsequently contributing to BSMC proliferation and migration. Moreover, inhibition of IL-8 signaling is a potential therapeutic target for YKL-40–induced inflammation and remodeling of asthma.

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“…particularly during exacerbation (27). YKL-40 has been shown to be secreted by bronchial macrophages and epithelium particularly in people with severe asthma (9) and allergen-sensitized mice (14).…”

Section: Discussionmentioning

confidence: 99%

Role of YKL-40 in Bronchial Smooth Muscle Remodeling in Asthma

Bara

Ozier²,

Girodet³

et al. 2012

Am J Respir Crit Care Med

113

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YKL-40 in asthmatic patients, and its correlations with exacerbation, eosinophils and immunoglobulin E

Cited by 90 publications

References 16 publications

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

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

YKL-40 Induces IL-8 Expression from Bronchial Epithelium via MAPK (JNK and ERK) and NF-κB Pathways, Causing Bronchial Smooth Muscle Proliferation and Migration

Role of YKL-40 in Bronchial Smooth Muscle Remodeling in Asthma

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