Background Chronic obstructive pulmonary disease （COPD） is a heterogeneous and complex disease of which the pathogenesis remains largely unknown. Many factors could influence COPD development and progression. One of them is the genetic risk factor. A severe hereditary deficiency of alpha-1 antitrypsin is the best genetic proof. Four single nucleotide polymorphisms （SNPs） of beta2-adrenergic receptor （β2AR） result in single amino acid substitution. Two loci had been extensively studied and found that they could change the function of β2AR. Two SNPs consist of substitutions of glycine for arginine at amino acid position 16, glutamic acid for glutamine at position 27. Many studies proved that polymorphisms at position 16 and 27 altered the lung function of COPD patients or the patient＇s susceptibility to the development of COPD. However, there was no exclusive conclusion. Therefore, a meta analysis was done to investigate the effect of polymorphisms in the 62-adrenergic receptor （ADRB2） gene on the risk of COPD and lung function. Methods Comprehensive searches of MEDLINE, Embase, Ovid, HighWire, Cochrane Library, and Chinese databases （CBMdisc, VIP, CNKI, and Wanfang data） from January 1980 to September 2011 were performed, using the keywords： COPD OR chronic obstructive pulmonary disease AND adrenoreceptor OR adrenergic receptor AND polymorphism OR mutation OR variation. Case-control research or cross sectional studies in which diagnosis of COPD met the Global Initiative for Chronic Obstructive Lung Disease （GOLD） guidelines; all the studies reported the ADRB2 genotype at position 16 or 27. Outcomes measured were genotype frequency and forced expiratory volume in the first second （FEV1%） in both the case and control. Results Twelve case-control studies and eight cross-sectional studies were included. Compared to the control （n= 1225）, neither Gly/Gly （n=527） nor Arg/Arg （n=422） homozygotes at position 16 demonstrated increased susceptibility to COPD, with odds ratios �
NIU Li-mingLIANG YingXU MingZHANG You-yiZHANG YuanHE Bei
Background The interleukin （IL）-32/tumor necrosis factor （TNF） a pathway is supposed to play a key role in the amplification of the immune response in chronic obstructive pulmonary disease （COPD） inflammation. Inhaled corticosteroids （ICS） in combination with long-acting I]2-agonists （LABA） have shown airway anti-inflammatory effects in recent studies, but the mechanism is still uncertain. Methods Patients were treated in a randomized, open-labeled, parallel group clinical trial with either a combination of salmeterol xinafoate/fluticasone propionate （SF; Seretide, GlaxoSmithKline） Diskus （50/500 pg twice daily） or ipratropium bromide/salbutamol （IS; Combivent, Boehringer Ingelheim） MDI （42 IJg/240 IJg quartic daily） for 12 weeks. At the start and the end of treatment, induced sputum was collected and the concentration of IL-32 and TNF-a, the number of neutrophUs and eosinophils were measured. Results Following 12 weeks of treatment, a statistically significant fall from baseline in the concentration of TNF-a in sputum （P=0.004） was seen after treatment with SF but not with IS. However, neither treatment had significant effects on the concentration of IL-32 in sputum. There was a decrease from baseline in the number of sputum neutrophils with SF that approached statistical significance （P=0.028） but not with IS, while the number of sputum eosinophils did not change significantly from baseline in either treatment group. There was a statistically significant decline from baseline in the quality of life as assessed by the St George＇s respiratory questionnaire in both the SF （P=0.004） and IS （P=0.030） treatment groups, but no evidence of improvement in lung function was observed in either group. Conclusion The sputum TNF-a and neutrophils, but not IL-32 and macrophages, could be reduced by ICS/LABA treatment, suggesting that IL-32 could be involved in the corticosteroid resistance of COPD inflammation.
