biostudies-literatureGane JMWest Midlands Chest FundMedical Research CouncilAcademy of Medical Sciences20https://www.ebi.ac.uk/biostudies/studies/S-EPMC4665865biostudies-literatureUnknown14<h4>Background</h4>Polymorphisms in the TNF-A gene have been associated with chronic obstructive pulmonary disease (COPD) in some case-control studies. Previous work has shown that COPD/chronic bronchitis subjects with alpha-1 antitrypsin deficiency with the rs361525 TNF-α single nucleotide polymorphism have 100 times more TNF-in spontaneous sputum than disease matched controls. Our objective was to determine if the presence of this polymorphism increased TNF-α production by blood monocytes from COPD subjects.<h4>Findings</h4>Monocytes from 18 COPD/alpha-1 antitrypsin deficient subjects, with and without the rs361525 polymorphism, were cultured in the presence or absence of lipopolysaccharide. Cell-free supernatants were analyzed by ELISA and real-time PCR performed using cDNA from extractJournal of negative results in biomedicineThe rs361525 polymorphism does not increase production of tumor necrosis factor alpha by monocytes from alpha-1 antitrypsin deficient subjects with chronic obstructive pulmonary disease - a pilot study.PMC4665865AMS-SGCL5-Sapey002013MR/L008335/1Sapey EGane JMStockley RAfalseThe rs361525 polymorphism does not increase production of tumor necrosis factor alpha by monocytes from alpha-1 antitrypsin deficient subjects with chronic obstructive pulmonary disease - a pilot study.<h4>Background</h4>Polymorphisms in the TNF-A gene have been associated with chronic obstructive pulmonary disease (COPD) in some case-control studies. Previous work has shown that COPD/chronic bronchitis subjects with alpha-1 antitrypsin deficiency with the rs361525 TNF-α single nucleotide polymorphism have 100 times more TNF-in spontaneous sputum than disease matched controls. Our objective was to determine if the presence of this polymorphism increased TNF-α production by blood monocytes from COPD subjects.<h4>Findings</h4>Monocytes from 18 COPD/alpha-1 antitrypsin deficient subjects, with and without the rs361525 polymorphism, were cultured in the presence or absence of lipopolysaccharide. Cell-free supernatants were analyzed by ELISA and real-time PCR performed using cDNA from extract2015-01-01T00:00:00Z2015 Dec2025-04-19T01:39:03.735Z2019-03-27T02:03:02ZS-EPMC46658652662097510.1186/s12952-015-0039-3