title: Interleukin-10 promoter polymorphism as risk factor to develop invasive pulmonary aspergillosis.
abstract: This present study was undertaken to examine the role of the host response to Aspergillus fumigatus in the development of clinical symptoms of invasive pulmonary aspergillosis (IPA). The natural outcome and response to IPA infection varies between individuals. Whereas some variation may be attributable to fungi and environmental variables, it is probable that host genetic background also plays a significant role. Interleukin (IL)-10 has a key function in the regulation of cellular immune responses and is involved in various inflammatory diseases. IL-10 promoter carries a polymorphism that has been associated to production levels. Our aim was to investigate the role of this polymorphism in susceptibility to develop IPA infection. The study included 120 haematological patients and 124 age and sex-matched controls and bi-allelic IL-10 -1082(G/A) polymorphism was examined. Genotypic (p=0.385) and allelic frequencies (p=0.527, OR=0.89, 95% CI=0.78-1.60) were similar between patients and healthy controls. IPA was diagnosed in 59 of the 120 patients according to consensus criteria published by the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group (EORTC/IFICG). Our results provide evidence that IL-10 -1082(AA) genotype is associated with resistance to develop IPA (p=0.001). Allele frequency of IL-10 -1082A allele was weakly associated with susceptibility to develop IPA infection (p=0.052). In conclusion, these results suggest that differential production of IL-10 may alter the risk for IPA in haematological patients.
authors.affiliation: Unidad de Investigación, Servicio de Hematología, Hospital Universitario Virgen de las Nieves, Centro Regional de Transfusión Sanguínea Granada-Almería, Edificio Licinio de la Fuente-Planta Sótano, Dr. Azpitarte, 4, 18012 Granada, Spain. jsainz@ugr.es
authors.forename: Juan
authors.initials: J
authors.lastname: Sainz
authors.forename: Laila
authors.initials: L
authors.lastname: Hassan
authors.forename: Eva
authors.initials: E
authors.lastname: Perez
authors.forename: Antonio
authors.initials: A
authors.lastname: Romero
authors.forename: Antonio
authors.initials: A
authors.lastname: Moratalla
authors.forename: Elisa
authors.initials: E
authors.lastname: López-Fernández
authors.forename: Salvador
authors.initials: S
authors.lastname: Oyonarte
authors.forename: Manuel
authors.initials: M
authors.lastname: Jurado
mesh_terms: D000328:Adult; D001228:Aspergillosis / Q000235:genetics* / Q000276:immunology; D005260:Female; D005690:Galactose / Q000031:analogs & derivatives; D020022:Genetic Predisposition to Disease; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics* / Q000276:immunology; D008172:Lung Diseases, Fungal / Q000235:genetics* / Q000276:immunology; D008297:Male; D008351:Mannans / Q000276:immunology; D008875:Middle Aged; D012150:Polymorphism, Restriction Fragment Length; D011401:Promoter Regions, Genetic; D011446:Prospective Studies
chemical_list: D008351:Mannans; C012990:galactomannan; D016753:Interleukin-10; D005690:Galactose