Tuesday, 6 December 2011
Poster Hall (Cancún Center)
Yuzaburo Inoue, MD, PhD
,
Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan
Naoki Shimojo, MD, PhD
,
Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan
Yoichi Suzuki, MD, PhD
,
Department of Public Health, Graduate School of Medicine, Chiba University, Chiba, Japan
Taiji Nakano, MD
,
Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan
Yoshinori Morita, MD, PhD
,
Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan
Takayasu Arima, MD, PhD
,
Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan
Minako Tomiita, MD, PhD
,
Department of Allergy and Rheumatology, Chiba Children's Hospital, Chiba, Japan
Yoichi Kohno, MD, PhD
,
Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japan
Background: Asthma is a chronic disease marked by airway hyperreactivity and inflammation. Although chitinase family members are induced in experimental models of asthma and in human asthmatics, their role in asthma pathogenesis remains controversial. YKL-39 and YKL-40 are members of human chitinase-like protein. Previously, it was shown that serum level of YKL-40 was higher in adult asthmatics but not in childhood asthmatics. However, association between another human chitinase-like protein YKL-39 and asthma or other allergic diseases have not been studied to date. To clarify if serum levels of YKL-39 and YKL-40 can be used as biomarkers of childhood asthma, in the present study, we measured serum levels of YKL-39 and YKL-40 in Japanese children.
Methods: This study was approved by the ethics committee of Chiba University. From 411 children whom we recruited at an elementary school attached to Chiba University and gave us informed consent, we selected, as control subjects (Control group), 115 who had never had any allergic diseases and did not have any aeroallergen-specific IgE. Fifteen subjects who had doctor-diagnosed asthma were selected as Bronchial Asthma (BA) group. As all subjects in BA group also had allergic rhinitis, we also selected, as another control, 30 who had allergic rhinitis but not doctor-diagnosed asthma (AR group). We collected serum from these subjects and measured serum levels of YKL-39 and YKL-40 by ELISA.
Results: In contrast to previous reports, we did not find any association between asthma and serum level of YKL-40. On the other hand, serum levels of YKL-39 in BA group were significantly lower than those in Control group or AR group, whereas those in AR group and Control group were identical.
Conclusions: Our data suggest that YKL-39 may have a protective role or be degraded in asthma pathogenesis, independently of atopic status. As we did not find the association between YKL-40 levels and asthma previously found in adult asthmatics, involvement of YKL-40 in asthma maybe different between ages.
