title: Proinflammatory and anti-inflammatory cytokine gene polymorphisms in hypersensitivity pneumonitis.
abstract: Hypersensitivity pneumonitis (HP) is an immunologically-mediated lung disease caused by repeated inhalation of dispersed antigen. Various cytokines have been reported to be involved in the immunopathogenesis of HP Recently, some reports suggested an association between the genetic control of cytokine production and disease susceptibility. To evaluate whether cytokine gene polymorphisms are associated with HP, we performed a case-control association study involving 61 patients with HP, consisting of summer-type HP (SHP) and bird fancier's lung (BFL, also named bird fancier's disease), as well as 101 healthy controls. Polymorphisms of the genes for tumor necrosis factor (TNF)-alpha (-308G/A, -857C/T, -863C/A, -1031T/C), interleukin (IL)-10 (-592C/A, -819C/T, -1082G/A), transforming growth factor (TGF)-beta1 (-509C/T, +869T/C), and IL-6 (-634C/G) were examined by restriction fragment length polymorphism analysis. There were no significant differences in allele frequency and genotype distribution among control, SHP, and BFL group. When HP group was divided into acute or chronic, no significant differences were detected between any groups. LPS-stimulated IL-6 secretion by whole blood cells was similar between subjects with GG genotype and non-GG genotype in IL-6 -634C/G polymorphism. In conclusion, the association between HP susceptibility and cytokine polymorphisms studied was not demonstrated.
authors.affiliation: Department of Integrated Pulmonology, Graduate School, Faculty of Medicine, Tokyo Medical and Dental University, Japan.
authors.forename: Kyoko
authors.initials: K
authors.lastname: Kondoh
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Usui
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Ohtani
authors.forename: Naohiko
authors.initials: N
authors.lastname: Inase
authors.forename: Shuji
authors.initials: S
authors.lastname: Miyake
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Yoshizawa
mesh_terms: D000542:Alveolitis, Extrinsic Allergic / Q000097:blood / Q000235:genetics*; D001716:Bird Fancier's Lung / Q000097:blood / Q000235:genetics; D016022:Case-Control Studies; D016207:Cytokines / Q000235:genetics*; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D018709:Statistics, Nonparametric; D016212:Transforming Growth Factor beta / Q000235:genetics; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D016207:Cytokines; D015850:Interleukin-6; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10