title: Toll-like receptor 2 gene polymorphisms Arg677Trp and Arg753Gln in chronic obstructive pulmonary disease.
abstract: Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide, with a continually rising mortality rate. As COPD is driven by abnormal pulmonary and systemic inflammation, Toll-like receptors (TLRs) seem to be important. TLRs play a key role in innate response, and in particular TLR2 gene polymorphisms Arg677Trp and Arg753Gln have been linked to an increased risk of infection. The purpose of this study was to investigate whether there is a link between polymorphisms in TLR2 and the onset or course of COPD. We analyzed 149 Caucasian COPD patients and 150 healthy individuals by using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) analysis. To further characterize the disease, patients were classified according to GOLD and divided into two subgroups comprising a stable (60/149) course and an unstable (89/149) course. The TLR2 Arg677Trp mutant allele was not found in any of the subjects. With a prevalence of 8.72% (13/149) for TLR2 Arg753Gln, the patients did not differ from the controls, with a prevalence of 10.67% (16/150). No significant difference was apparent (P = 0.571). None of the individuals showed homozygosity for TLR2 Arg753Gln. With regard to the course of COPD, the prevalence of TLR2 Arg753Gln in the control group did not differ significantly either from the stable subgroup (P = 0.196) or from the unstable subgroup (P = 0.891). Our results suggest that there is no association of the TLR2 polymorphisms Arg677Trp and Arg753Gln with either the onset or the course of COPD.
authors.affiliation: Department of Pneumology, Medical Clinic II, University of Bonn, Sigmund-Freud-Strasse 25, Bonn, Germany. stefan.pabst@ukb.uni-bonn.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Pabst
authors.forename: Vildan
authors.initials: V
authors.lastname: Yenice
authors.forename: Martina
authors.initials: M
authors.lastname: Lennarz
authors.forename: Izabela
authors.initials: I
authors.lastname: Tuleta
authors.forename: Georg
authors.initials: G
authors.lastname: Nickenig
authors.forename: Adrian
authors.initials: A
authors.lastname: Gillissen
authors.forename: Christian
authors.initials: C
authors.lastname: Grohé
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D054458:Amplified Fragment Length Polymorphism Analysis; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012150:Polymorphism, Restriction Fragment Length; D029424:Pulmonary Disease, Chronic Obstructive / Q000175:diagnosis / Q000208:ethnology / Q000235:genetics* / Q000276:immunology; D012307:Risk Factors; D012720:Severity of Illness Index; D051195:Toll-Like Receptor 2 / Q000235:genetics*; D044465:White People / Q000235:genetics
chemical_list: C495342:TLR2 protein, human; D051195:Toll-Like Receptor 2