title: Overexpression of CD-11b and CXCR1 on circulating neutrophils: its possible role in COPD.
abstract: BACKGROUND
  It has been shown that the beta2-integrin molecule is up-regulated in circulating neutrophils in COPD subjects. However, little has been reported about the expression of the cell surface molecules in such patients and their relationship with pulmonary function. The aim of the present study was to investigate the surface expression of molecules in circulating neutrophils and to clarify their possible role in the airflow limitation of COPD.
  
  
  METHODS
  The surface expression of Mac-1 cells (ie, CD-11b and CD-18 cells) and CXC chemokine receptor (CXCR) 1 and CXCR2 of circulating neutrophils obtained from COPD patients and healthy subjects (HSs) was measured by flow cytometry analysis. The serum levels of interleukin (IL)-8 were measured by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Both CD-11b and CXCR1 expression were significantly higher in COPD patients than in HSs (mean [+/- SE] CD-11b concentration: HSs, 9.7 +/- 1.0; COPD patients, 14.2 +/- 1.8 [p < 0.05]; mean CXCR1 concentration: HSs, 9.6 +/- 0.5; COPD patients, 11.9 +/- 0.4 [p < 0.01]). Although aging was positively correlated with the expression of CXCR1 (r = 0.440; p < 0.01), none of the other background factors, including smoking and body mass index, showed a correlation with the expression of the molecules. Although serum IL-8 levels were higher in patients with COPD than in HSs, no significant correlation between serum IL-8 levels and the expression of any molecule was seen. The expression of CD-11b (r = -0.317) and CXCR1 (r = -0.383) showed a significant negative correlation with the severity of airflow limitation (both p < 0.05).
  
  
  CONCLUSIONS
  The overexpression of CD-11b and CXCR1 in circulating neutrophils may be associated with the development of airflow limitation in COPD patients.
authors.affiliation: Third Department of Internal Medicine, Wakayama Medical University, School of Medicine, 811-1 Kimiidera, Wakayama 641-8509, Japan.
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Yamagata
authors.forename: Hisatoshi
authors.initials: H
authors.lastname: Sugiura
authors.forename: Tomonori
authors.initials: T
authors.lastname: Yokoyama
authors.forename: Satoru
authors.initials: S
authors.lastname: Yanagisawa
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Ichikawa
authors.forename: Kazuhito
authors.initials: K
authors.lastname: Ueshima
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Akamatsu
authors.forename: Tsunahiko
authors.initials: T
authors.lastname: Hirano
authors.forename: Masanori
authors.initials: M
authors.lastname: Nakanishi
authors.forename: Yuko
authors.initials: Y
authors.lastname: Yamagata
authors.forename: Kazuto
authors.initials: K
authors.lastname: Matsunaga
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Minakata
authors.forename: Masakazu
authors.initials: M
authors.lastname: Ichinose
mesh_terms: D000368:Aged; D039481:CD11b Antigen / Q000097:blood*; D018821:CD18 Antigens / Q000097:blood*; D016022:Case-Control Studies; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000503:physiopathology; D023062:Receptors, Interleukin-8A / Q000097:blood*; D023063:Receptors, Interleukin-8B / Q000097:blood*; D014109:Total Lung Capacity / Q000502:physiology
chemical_list: D039481:CD11b Antigen; D018821:CD18 Antigens; C509295:ITGAM protein, human; D016209:Interleukin-8; D023062:Receptors, Interleukin-8A; D023063:Receptors, Interleukin-8B