title: Impaired systemic cell-mediated immunity and increased susceptibility to acute respiratory tract infections in patients with COPD.
abstract: Although it has been reported that chronic obstructive pulmonary disease (COPD) is frequently associated with systemic immune disturbances, negative impact of these disturbances on the increased prevalence of acute respiratory tract infections (aRTIs) has remained unclear. We evaluated circulating levels of interferon-gamma (IFN-gamma), soluble interleukin-2 receptor (sIL-2R), neopterin, and soluble intercellular adhesion molecule-1 (sICAM-1) in 35 clinically stable patients with COPD and in 22 age-matched healthy controls, since these molecules are considered to reflect the in vivo status of systemic cell-mediated immunity (CMI). We found that circulating levels of sIL-2R (1.52+/-1.25 vs. 0.97+/-0.48 ng/ml; P<0.05), neopterin (7.23+/-4.24 vs. 4.95+/-1.52 nmol/l; P<0.05), and sICAM-1 (665+/-302 vs. 328+/-164 ng/ml; P<0.0001), but not IFN-gamma (7.55+/-4.72 vs. 6.65+/-1.13 pg/ml; P=NS) were significantly higher in patients with COPD than in the controls. Importantly, follow-up study for 12 months demonstrated that patients in subgroup with relatively higher circulating levels of sIL-2R (2.20+/-1.44 ng/ml, n=18) had significantly higher risk of developing aRTIs (P=0.0204) than those in subgroup with relatively lower circulating levels of sIL-2R (0.80+/-0.23 ng/ml, n=17). These results may suggest that impaired systemic CMI observed in COPD patients is associated with the increased susceptibility to aRTIs in these patients.
authors.affiliation: First Department of Internal Medicine, School of Medicine, Yamagata University, 2-2-2, Iida-Nishi, Yamagata 990 9585, Japan. takabata@med.id.yamagata-u.ac.jp
authors.forename: Noriaki
authors.initials: N
authors.lastname: Takabatake
authors.forename: Makoto
authors.initials: M
authors.lastname: Sata
authors.forename: Shuichi
authors.initials: S
authors.lastname: Abe
authors.forename: Sumito
authors.initials: S
authors.lastname: Inoue
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Saito
authors.forename: Hideki
authors.initials: H
authors.lastname: Yuki
authors.forename: Yoko
authors.initials: Y
authors.lastname: Shibata
authors.forename: Isao
authors.initials: I
authors.lastname: Kubota
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D016207:Cytokines / Q000378:metabolism*; D004198:Disease Susceptibility / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D007154:Immune System Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D007111:Immunity, Cellular; D008297:Male; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D012141:Respiratory Tract Infections / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D014797:Vital Capacity / Q000502:physiology
chemical_list: D016207:Cytokines; D010100:Oxygen