title: Involvement of TNFalpha -308A promoter polymorphism in the development of asthma in children infected with Chlamydophila pneumoniae.
abstract: Several data indicate a connection between Chlamydophila pneumoniae infection and asthma. Although C. pneumoniae is a common cause of infection, not all infected patients develop asthma. This suggests that certain individuals may be genetically predisposed to the chronic effects of C. pneumoniae infection on airway functions. We investigated the possible modifying effect of different polymorphisms on C. pneumoniae infection and on the susceptibility to asthma in 318 children, among those 144 had asthma and 174 had no asthmatic symptoms. C. pneumoniae-specific antibodies were measured by ELISA. Tumor necrosis factor-alpha (TNFalpha), monocyte chemoattractant protein-1 (MCP-1), and RANTES (regulated on activation normal T cell expressed and secreted) genotypes were determined by PCR-restriction fragment length polymorphism (RFLP). There were no significant differences in the percentage of children positive for C. pneumoniae-specific antibodies between cases and controls. None of the genotypes was associated with altered susceptibility to C. pneumoniae infection. Among asthmatic children carrying the TNFalpha -308A allele, there were significantly more patients positive for C. pneumoniae-specific IgG, than among control children carrying the same allele (20.1% versus 9.2% of asthmatic versus control children, respectively; p = 0.002; odds ratio = 3.52 (1.52-7.53); p = 0.005). This study indicates the possible roles of polymorphisms in the immune system in the susceptibility to asthma in children infected with C. pneumoniae.
authors.affiliation: Department of Genetics, Cell and Immunobiology, Semmelweis University, H-1089, Budapest, Hungary.
authors.forename: Gergely
authors.initials: G
authors.lastname: Tölgyesi
authors.forename: Márton
authors.initials: M
authors.lastname: Keszei
authors.forename: Ildikó
authors.initials: I
authors.lastname: Ungvári
authors.forename: Adrienne
authors.initials: A
authors.lastname: Nagy
authors.forename: András
authors.initials: A
authors.lastname: Falus
authors.forename: Csaba
authors.initials: C
authors.lastname: Szalai
mesh_terms: D000293:Adolescent; D000906:Antibodies / Q000097:blood; D001249:Asthma / Q000209:etiology / Q000235:genetics / Q000276:immunology; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D018946:Chemokine CCL5 / Q000235:genetics / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D023521:Chlamydophila Infections / Q000150:complications / Q000276:immunology; D016993:Chlamydophila pneumoniae / Q000276:immunology*; D004198:Disease Susceptibility; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D012044:Regression Analysis; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics* / Q000378:metabolism
chemical_list: D000906:Antibodies; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D018946:Chemokine CCL5; D014409:Tumor Necrosis Factor-alpha