Heidi Hyytiäinen1, Pirkka V Kirjavainen2, Martin Täubel1, Pauli Tuoresmäki1, Lidia Casas3, Joachim Heinrich4, Gunda Herberth5, Marie Standl6, Harald Renz7, Eija Piippo-Savolainen8, Anne Hyvärinen1, Juha Pekkanen9, Anne M Karvonen10. 1. Department of Health Security, Finnish Institute for Health and Welfare, Kuopio, Finland. 2. Department of Health Security, Finnish Institute for Health and Welfare, Kuopio, Finland; Institute of Public Health and Clinical Nutrition, Department of Clinical Nutrition, University of Eastern Finland, Kuopio, Finland. 3. Centre for Environment and Health - Department of Public Health and Primary Care, KU Leuven, Leuven, Belgium; Social Epidemiology and Health Policy, Department of Family Medicine and Population Health, University of Antwerp, Antwerp, Belgium. 4. Institute of Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany; Institute and Outpatient Clinic for Occupational, Social and Environmental Medicine, University Hospital Munich, Ludwig Maximillians University Munich, Member of German Center for Lung Research (DZL), Munich, Germany. 5. Department of Environmental Immunology/Core Facility Studies, Helmholtz Centre for Environmental Research- UFZ, Leipzig, Germany. 6. Institute of Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany. 7. Department of Clinical Chemistry and Molecular Diagnostics, Philipps University of Marburg, Marburg, Germany; Member of the German Center for Lung Research, Germany. 8. Department of Pediatrics, Kuopio University Hospital, Kuopio, Finland; Department of Pediatrics, University of Eastern Finland, Kuopio; Finland. 9. Department of Health Security, Finnish Institute for Health and Welfare, Kuopio, Finland; Department of Public Health, University of Helsinki, Helsinki, Finland. 10. Department of Health Security, Finnish Institute for Health and Welfare, Kuopio, Finland. Electronic address: anne.karvonen@thl.fi.
Abstract
BACKGROUND: Microbial exposures in early childhood direct the development of the immune system and their diversity may influence the risk of allergy development. We aimed to determine whether the indoor microbial diversity at early-life is associated with the development of allergic rhinitis and inhalant atopy. METHODS: The study population included children within two birth cohorts: Finnish rural-suburban LUKAS (N = 312), and German urban LISA from Munich and Leipzig study centers (N = 248). The indoor microbiota diversity (Chao1 richness and Shannon entropy) was characterized from floor dust samples collected at the child age of 2-3 months by Illumina MiSeq sequencing of bacterial and fungal DNA amplicons. Allergic rhinitis and inhalant atopy were determined at the age of 10 years and analyzed using logistic regression models. RESULTS: High bacterial richness (aOR 0.19, 95%CI 0.09-0.42 for middle and aOR 0.12, 95%CI 0.05-0.29 for highest vs. lowest tertile) and Shannon entropy were associated with lower risk of allergic rhinitis in LISA, and similar trend was seen in LUKAS. We observed some significant associations between bacterial and fungal diversity measured and the risk of inhalant atopy, but the associations were inconsistent between the two cohorts. High bacterial diversity tended to be associated with increased risk of inhalant atopy in rural areas, but lower risk in more urban areas. Fungal diversity tended to be associated with increased risk of inhalant atopy only in LISA. CONCLUSIONS: Our study suggests that a higher bacterial diversity may reduce the risk of allergic rhinitis later in childhood. The environment-dependent heterogeneity in the associations with inhalant atopy - visible here as inconsistent results between two differing cohorts - suggests that specific constituents of the diversity may be relevant.
BACKGROUND: Microbial exposures in early childhood direct the development of the immune system and their diversity may influence the risk of allergy development. We aimed to determine whether the indoor microbial diversity at early-life is associated with the development of allergic rhinitis and inhalant atopy. METHODS: The study population included children within two birth cohorts: Finnish rural-suburban LUKAS (N = 312), and German urban LISA from Munich and Leipzig study centers (N = 248). The indoor microbiota diversity (Chao1 richness and Shannon entropy) was characterized from floor dust samples collected at the child age of 2-3 months by Illumina MiSeq sequencing of bacterial and fungal DNA amplicons. Allergic rhinitis and inhalant atopy were determined at the age of 10 years and analyzed using logistic regression models. RESULTS:High bacterial richness (aOR 0.19, 95%CI 0.09-0.42 for middle and aOR 0.12, 95%CI 0.05-0.29 for highest vs. lowest tertile) and Shannon entropy were associated with lower risk of allergic rhinitis in LISA, and similar trend was seen in LUKAS. We observed some significant associations between bacterial and fungal diversity measured and the risk of inhalant atopy, but the associations were inconsistent between the two cohorts. High bacterial diversity tended to be associated with increased risk of inhalant atopy in rural areas, but lower risk in more urban areas. Fungal diversity tended to be associated with increased risk of inhalant atopy only in LISA. CONCLUSIONS: Our study suggests that a higher bacterial diversity may reduce the risk of allergic rhinitis later in childhood. The environment-dependent heterogeneity in the associations with inhalant atopy - visible here as inconsistent results between two differing cohorts - suggests that specific constituents of the diversity may be relevant.