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

Adlerberth, Ingegerd; Strachan, David P.; Matricardi, Paolo M.; Ahrné, Siv LU ; Orfei, Lia; Aberg, Nils; Perkin, Michael R.; Tripodi, Salvatore; Hesselmar, Bill and Saalman, Robert, et al. (2007) In Journal of Allergy and Clinical Immunology 120(2). p.343-350
Abstract
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 Goteborg (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... (More)
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 Goteborg (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. (Less)
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published
subject
keywords
atopic eczema, allergy, sensitization, IgE, intestine, commensal, infant, bacteria
in
Journal of Allergy and Clinical Immunology
volume
120
issue
2
pages
343 - 350
publisher
Elsevier
external identifiers
  • wos:000248654900019
  • scopus:34547128871
ISSN
1097-6825
DOI
10.1016/j.jaci.2007.05.018
language
English
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yes
id
c010605f-05df-406b-989c-235eb62e8797 (old id 646437)
date added to LUP
2007-12-11 11:06:32
date last changed
2017-11-12 03:56:28
@article{c010605f-05df-406b-989c-235eb62e8797,
  abstract     = {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 Goteborg (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.},
  author       = {Adlerberth, Ingegerd and Strachan, David P. and Matricardi, Paolo M. and Ahrné, Siv and Orfei, Lia and Aberg, Nils and Perkin, Michael R. and Tripodi, Salvatore and Hesselmar, Bill and Saalman, Robert and Coates, Anthony R. and Bonanno, Carmen L. and Panetta, Valentina and Wold, Agnes E.},
  issn         = {1097-6825},
  keyword      = {atopic eczema,allergy,sensitization,IgE,intestine,commensal,infant,bacteria},
  language     = {eng},
  number       = {2},
  pages        = {343--350},
  publisher    = {Elsevier},
  series       = {Journal of Allergy and Clinical Immunology},
  title        = {Gut microbiota and development of atopic eczema in 3 European birth cohorts},
  url          = {http://dx.doi.org/10.1016/j.jaci.2007.05.018},
  volume       = {120},
  year         = {2007},
}