Lasse Ruokolainen1, Anna Parkkola2,3, Antti Karkman1,4, Hanna Sinkko5,6, Aleksandr Peet7, Anu-Maaria Hämäläinen8, Leena von Hertzen9, Vallo Tillmann7, Katriina Koski10, Suvi M Virtanen11,12,13, Onni Niemelä14, Tari Haahtela9, Mikael Knip2,3,13,15. 1. Department of Biosciences, University of Helsinki, Helsinki, Finland. 2. Pediatric Research Center, Children's Hospital, Helsinki University Hospital, University of Helsinki, Helsinki, Finland. 3. Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland. 4. Department of Microbiology, University of Helsinki, Helsinki, Finland. 5. Human Microbiome (HUMI) Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland. 6. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden. 7. Department of Paediatrics, Tartu University Hospital, University of Tartu, Tartu, Estonia. 8. Department of Paediatrics, Jorvi Hospital, Helsinki University Hospital, Espoo, Finland. 9. Skin and Allergy Hospital, Helsinki University Hospital, Helsinki, Finland. 10. Clinicum, Faculty of Medicine, University of Helsinki, Helsinki, Finland. 11. Department of Public Health Solutions, National Institute for Health and Welfare, Helsinki, Finland. 12. Faculty of Social Sciences/Health Sciences, University of Tampere, Tampere, Finland. 13. Center for Child Health Research, Tampere University Hospital and Science Centre, Tampere University Hospital, University of Tampere, Tampere, Finland. 14. Department of Laboratory Medicine and Medical Research Unit, Seinäjoki Central Hospital, University of Tampere, Tampere, Finland. 15. Folkhälsan Research Center, Helsinki, Finland.
Abstract
BACKGROUND: Allergic diseases are more common in Finland than in Estonia, which-according to the biodiversity hypothesis-could relate to differences in early microbial exposures. METHODS: We aimed at defining possible microbial perturbations preceding early atopic sensitization. Stool, nasal and skin samples of 6-month-old DIABIMMUNE study participants with HLA susceptibility to type 1 diabetes were collected. We compared microbiotas of sensitized (determined by specific IgE results at 18 months of age) and unsensitized Estonian and Finnish children. RESULTS: Sensitization was differentially targeted between populations, as egg-specific and birch pollen-specific IgE was more common in Finland. Microbial diversity and community composition also differed; the genus Acinetobacter was more abundant in Estonian skin and nasal samples. Particularly, the strain-level profile of Acinetobacter lwoffii was more diverse in Estonian samples. Early microbiota was not generally associated with later sensitization. Microbial composition tended to differ between children with or without IgE-related sensitization, but only in Finland. While land-use pattern (ie green areas vs. urban landscapes around the children's homes) was not associated with microbiota as a whole, it associated with the composition of the genus Acinetobacter. Breastfeeding affected gut microbial composition and seemed to protect from sensitization. CONCLUSIONS: In accordance with the biodiversity hypothesis, our results support disparate early exposure to environmental microbes between Finnish and Estonian children and suggest a significant role of the genus Acinetobacter in the allergy gap between the two populations. The significance of the observed differences for later allergic sensitization remains open.
BACKGROUND:Allergic diseases are more common in Finland than in Estonia, which-according to the biodiversity hypothesis-could relate to differences in early microbial exposures. METHODS: We aimed at defining possible microbial perturbations preceding early atopic sensitization. Stool, nasal and skin samples of 6-month-old DIABIMMUNE study participants with HLA susceptibility to type 1 diabetes were collected. We compared microbiotas of sensitized (determined by specific IgE results at 18 months of age) and unsensitized Estonian and Finnish children. RESULTS: Sensitization was differentially targeted between populations, as egg-specific and birch pollen-specific IgE was more common in Finland. Microbial diversity and community composition also differed; the genus Acinetobacter was more abundant in Estonian skin and nasal samples. Particularly, the strain-level profile of Acinetobacter lwoffii was more diverse in Estonian samples. Early microbiota was not generally associated with later sensitization. Microbial composition tended to differ between children with or without IgE-related sensitization, but only in Finland. While land-use pattern (ie green areas vs. urban landscapes around the children's homes) was not associated with microbiota as a whole, it associated with the composition of the genus Acinetobacter. Breastfeeding affected gut microbial composition and seemed to protect from sensitization. CONCLUSIONS: In accordance with the biodiversity hypothesis, our results support disparate early exposure to environmental microbes between Finnish and Estonian children and suggest a significant role of the genus Acinetobacter in the allergy gap between the two populations. The significance of the observed differences for later allergic sensitization remains open.