The 8.1 ancestral MHC haplotype is associated with delayed onset of colonization in cystic fibrosis

Judit Laki, István Laki, Krisztina Németh, Rita Újhelyi, Olga Bede, Emoke Endreffy, Katalin Bolbás, Kálmán Gyurkovits, Eszter Csiszér, Eniko Sólyom, Gergely Dobra, Adrienn Halász, Éva Pozsonyi, Katalin Rajczy, Zoltán Prohászka, György Fekete, George Füst

Research output: Article

27 Citations (Scopus)

Abstract

Major cause of death in patients with cystic fibrosis (CF) is colonization with Staphylococcus aureus and Pseudomonas aeruginosa. The wide phenotypic variation in CF patients suggests that genes other than the cystic fibrosis transmembrane conductance regulator (CFTR) gene modify the disease. The 8.1 ancestral haplotype (8.1AH) in main histocompatibility complex is associated with alterations of the immune response. To study the influence of carriage of 8.1AH on frequency and onset of colonization in CF patients, DNA samples of 72 CF patients (39 homozygous and 33 heterozygous for ΔF508) were genotyped for member alleles of the 8.1AH: HLA-DQB1*0201, HLA-DRB1*0301, receptor for advanced glycation end products (AGER) - 429C, HSP70-2 -1267G (HSP70-2G) and tumor necrosis factor-α (TNF- α) -308A (TNF2). Colonization was verified by regular clinical and bacteriological screening. Frequency of colonization was significantly (P = 0.012) lower in the 8.1AH carriers; age, gender and ΔF508 genotype-adjusted odds ratio to be colonized of the carriers versus non-carriers was 0.112 (0.024-0.520). According to survival analysis, patients with 8.1AH had significantly (P < 0.0001) longer colonization-free period compared with non-carriers. Our novel observations demonstrate that the 8.1AH is associated with delayed onset of colonization in CF, presumably by influencing defense mechanisms against infections.

Original languageEnglish
Pages (from-to)1585-1590
Number of pages6
JournalInternational Immunology
Volume18
Issue number11
DOIs
Publication statusPublished - nov. 2006

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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