title: Sputum YKL-40 levels and pathophysiology of asthma and chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Recent evidence suggests that YKL-40, also called chitinase-3-like-1 protein, is involved in the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD). Details of sputum YKL-40 in asthma and COPD, however, remain unknown.
  
  
  OBJECTIVE
  To clarify associations of sputum YKL-40 levels with clinical indices in asthma and COPD.
  
  
  METHODS
  Thirty-nine patients with asthma, 14 age-matched never-smokers as controls, 45 patients with COPD, and 7 age-matched smokers as controls were recuited for this study. Sputum YKL-40 levels were measured and YKL-40 expression in sputum cells was evaluated by immunocytochemistry.
  
  
  RESULTS
  Sputum YKL-40 levels were higher in patients with COPD (346 ± 325 ng/ml) than in their smoker controls (125 ± 122 ng/ml; p < 0.05), but were not significantly different between patients with asthma (117 ± 170 ng/ml) and their controls (94 ± 44 ng/ml; p = 0.15). In patients with asthma only, sputum YKL-40 levels were positively correlated with disease severity (r = 0.34, p = 0.034) and negatively correlated with pre- and postbronchodilator %FEV(1) (r = -0.47 and -0.42, respectively; p < 0.01) and forced mid-expiratory flow (r = -0.48 and -0.46, respectively, p < 0.01). Sputum YKL-40 levels were positively correlated with sputum neutrophil counts in asthma (r = 0.55, p < 0.001) and with neutrophil and macrophage counts in COPD (r = 0.45 and 0.65, respectively, p < 0.01). YKL-40 was expressed in the cytoplasm of sputum neutrophils and macrophages in all groups.
  
  
  CONCLUSIONS
  Elevated sputum YKL-40 reflects airflow obstruction in asthma whereas the roles of YKL-40 in the proximal airways in COPD remain to be elucidated.
authors.affiliation: Department of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Kojiro
authors.initials: K
authors.lastname: Otsuka
authors.forename: Hisako
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Akio
authors.initials: A
authors.lastname: Niimi
authors.forename: Shigeo
authors.initials: S
authors.lastname: Muro
authors.forename: Isao
authors.initials: I
authors.lastname: Ito
authors.forename: Tomoshi
authors.initials: T
authors.lastname: Takeda
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Terada
authors.forename: Masafumi
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Matsuoka
authors.forename: Makiko
authors.initials: M
authors.lastname: Jinnai
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Oguma
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Nakaji
authors.forename: Hideki
authors.initials: H
authors.lastname: Inoue
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tajiri
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Iwata
authors.forename: Kazuo
authors.initials: K
authors.lastname: Chin
authors.forename: Michiaki
authors.initials: M
authors.lastname: Mishima
mesh_terms: D054392:Adipokines / Q000378:metabolism*; D000328:Adult; D000368:Aged; D001249:Asthma / Q000378:metabolism / Q000503:physiopathology*; D000071451:Chitinase-3-Like Protein 1; D003430:Cross-Sectional Studies; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007073:Immunoglobulin E / Q000032:analysis; D037102:Lectins / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism / Q000503:physiopathology*; D013183:Sputum / Q000378:metabolism*
chemical_list: D054392:Adipokines; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D037102:Lectins; D007073:Immunoglobulin E