ABSTRACT
Chronic obstructive pulmonary disease (COPD) is an inflammation disorder and possibly an autoimmune disease. The components of the autoimmune response in the circulatory system are of considerable interest to clinicians. Because aberrations of costimulation status have been noted in COPD, the presence of autoantibodies to B7 costimulatory factor CD80 were investigated in a cohort of patients. Recombinant rs1CD80 (lacking the transmembrane domain of CD80) was used for Western blot analysis and ELISA to investigate the presence of autoantibodies in sera of patients with stable COPD and in controls without COPD. Cytokines IL-6 and IL-8 were detected using ELISA. Western blot revealed a specific band reacting to rs1CD80 by diluting sera pool of patients, which indicated the existence of autoantibodies to CD80. The serum level of anti-rs1CD80 was higher in patients with COPD than in controls(P=0.0185) and was positively correlated to the serum level of IL-6 (r=0.797, P<0.001) and IL-8 (r=0.608, P<0.001). There was a tendency that more higher level of anti-rs1CD80, more severe COPD stage. The existence of autoantibodies to costimulatory factor CD80 may suggest a pathogenic role of costimulatory factors in COPD.
ABSTRACT
Previous in vitro studies have demonstrated that resveratrol is able to significantly inhibit the upregulation of mucin 5AC (MUC5AC), a major component of mucus; thus indicating that resveratrol may have potential in regulating mucus overproduction. However, there have been few studies regarding the resveratrolmediated prevention of MUC5AC overproduction in vivo, and the mechanisms by which resveratrol regulates MUC5AC expression have yet to be elucidated. In the present study, an ovalbumin (OVA)challenged murine model of asthma was used to assess the effects of resveratrol treatment on mucus production in vivo. The results demonstrated that resveratrol significantly inhibited OVAinduced airway inflammation and mucus production. In addition, the mRNA and protein expression levels of MUC5AC were increased in the OVAchallenged mice, whereas treatment with resveratrol significantly inhibited this effect. The expression levels of murine calciumactivated chloride channel (mCLCA)3, an important key mediator of MUC5AC production, were also reduced following resveratrol treatment. Furthermore, in vitro studies demonstrated that resveratrol significantly inhibited human (h)CLCA1 and MUC5AC expression in a dosedependent manner. These results indicated that resveratrol was effective in preventing mucus overproduction and MUC5AC expression in vivo, and its underlying mechanism may be associated with regulation of the mCLCA3/hCLCA1 signaling pathway.
