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Gut microbiota and development of atopic eczema in 3 European birth cohorts.

Journal article
Authors Ingegerd Adlerberth
David P Strachan
Paolo M Matricardi
Siv Ahrné
Lia Orfei
Nils Åberg
Michael R Perkin
Salvatore Tripodi
Bill Hesselmar
Robert Saalman
Anthony R Coates
Carmen L Bonanno
Valentina Panetta
Agnes E Wold
Published in The Journal of allergy and clinical immunology
Volume 120
Issue 2
Pages 343-50
ISSN 0091-6749
Publication year 2007
Published at Institute of Biomedicine, Department of Infectious Medicine
Institute of Clinical Sciences
Pages 343-50
Language en
Keywords Aging, immunology, Allergens, immunology, Bacteroides, growth & development, Bifidobacterium, growth & development, Cesarean Section, Clostridium, growth & development, Cohort Studies, Colony Count, Microbial, Dermatitis, Atopic, immunology, microbiology, Escherichia coli, growth & development, Europe, Feces, microbiology, Female, Food Hypersensitivity, blood, immunology, microbiology, Humans, Immunoglobulin E, blood, Infant, Newborn, Life Style, Longitudinal Studies, Male, Rectum, microbiology, Risk Factors
Subject categories Medical and Health Sciences


BACKGROUND: Stimulation of the immune system by gut microbes might prevent allergy development. OBJECTIVE: The present study examined the hypothesis that sensitization to food allergens and atopic eczema are influenced by the infantile intestinal colonization pattern. METHODS: Infants were recruited perinatally in Göteborg (n = 116), London (n = 108), and Rome (n = 100). Commensal bacteria were identified to the genus or species level in rectal (3 days) and quantitative stool cultures (7, 14, and 28 days and 2, 6, and 12 months of age). At 18 months of age, atopic eczema and total and food-specific IgE levels were assessed. These outcomes were modeled in relation to time to colonization with 11 bacterial groups and to ratios of strict anaerobic to facultative anaerobic bacteria and gram-positive to gram-negative bacteria at certain time points. Study center, mode of delivery, parity, and infant diet were included as covariates. RESULTS: Neither atopic eczema nor food-specific IgE by 18 months of age were associated with time of acquisition of any particular bacterial group. Cesarean section delayed colonization by Escherichia coli and Bacteroides and Bifidobacterium species, giving way to, for example, Clostridium species. Lack of older siblings was associated with earlier colonization by Clostridium species and lower strict anaerobic/facultative anaerobic ratio at 12 months. CONCLUSIONS: This study does not support the hypothesis that sensitization to foods or atopic eczema in European infants in early life is associated with lack of any particular culturable intestinal commensal bacteria. CLINICAL IMPLICATIONS: The nature of the microbial stimulus required for protection from allergy remains to be identified.

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