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PS-323 The Gene Polymorphism Of Il-17 G-152a Is Associated With Increased Colonisation Of Streptococcus Pneumoniae In Children
  1. J Vuononvirta1,
  2. V Peltola2,
  3. J Ilonen3,
  4. Q He1
  1. 1Department of Infectious Disease Surveillance and Control, National Institute for Health and Welfare, Turku, Finland
  2. 2Department of Pediatric, Turku University Hospital, Turku, Finland
  3. 3Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland


Background and aims Streptococcus pneumoniae is a common respiratory pathogen and up to 50% of children acquire S. pneumoniae in their nasopharynx during the first 12 months of life. The cytokine interleukin-17A (IL-17A) plays an important role in host defense against extracellular bacterial pathogens. We investigated the effect of IL-17 G-152A polymorphism on pneumococcal colonisation and the serum level of IL-17A in children.

Methods Nasopharyngeal swabs (NP) and blood samples were collected from 412 Finnish children at 2.6 months. Of them, 160 had both NP and blood sample available at 12 and 24 months of age. The semi-quantitative culture method was used for bacterial culture, Sequenom iPlex Gold System for IL-17A genotyping and Luminex 200 for serum IL-17A determination.

Results Of 160 subjects, 34% were G/G wild type, 45% G/A heterozygotes and 21% A/A homozygotes. The prevalence of S. pneumoniae in the same cohort of 160 subjects increased from 8% to 30% during the 2-year follow-up. Significantly higher pneumococcal colonisation was found in subjects with A/A genotype at both 12 and 24 months of age compared to those with G/G (p < 0.05 for both). Of 96 sera randomly selected from 160 subjects at 12 months, only 6% with A/A and 33% with G/A genotypes had detectable IL-17A compared to 75% with G/G (p < 0.001, p < 0.01).

Conclusions Our data suggest that gene polymorphism of IL-17 G-152A is associated with increased colonisation of S. pneumoniae and that lower serum levels of IL-17A were observed in subjects with A/A and G/A genotypes of IL-17A.

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