Reduced diversity in the early fecal microbiota of infants with atopic eczema

Received 4 June 2007; received in revised form 5 September 2007; accepted 10 September 2007. published online 29 October 2007.

Background

It might be that early intestinal colonization by bacteria in westernized infants fails to give rise to sufficient immune stimulation to support maturation of regulatory immune mechanisms.

Objective

The purpose of the present study was to characterize the very early infantile microbiota by using a culture-independent approach and to relate the colonization pattern to development of atopic eczema in the first 18 months of life.

Methods

Fecal samples were collected from 35 infants at 1 week of age. Twenty infants were healthy, and 15 infants were given diagnoses of atopic eczema at the age of 18 months. The fecal microbiota of the infants was compared by means of terminal restriction fragment length polymorphism (T-RFLP) and temporal temperature gradient gel electrophoresis (TTGE) analysis of amplified 16S rRNA genes.

Results

By means of T-RFLP analysis, the median number of peaks, Shannon-Wiener index, and Simpson index of diversity were significantly less for infants with atopic eczema than for infants remaining healthy in the whole group and for the Swedish infants when AluI was used for digestion. The same was found when TTGE patterns were compared. In addition, TTGE analysis showed significantly less bands and lower diversity indices for the British atopic infants compared with those of the control subjects.

Conclusion

There is a reduced diversity in the early fecal microbiota of infants with atopic eczema during the first 18 months of life.

Key words: Atopic eczema, intestinal microbiota, diversity, terminal restriction fragment length polymorphism, temporal temperature gradient gel electrophoresis

Abbreviations used: Cy5, Indodicarbocyanine, T-RF, Terminal restriction fragment, T-RFLP, Terminal restriction fragment length polymorphism, TTGE, Temporal temperature gradient gel electrophoresis

a Department of Food Technology, Engineering and Nutrition, Lund University, Lund, Sweden

b Department of Clinical Bacteriology, Göteborg University, Göteborg, Sweden

e Department of Paediatrics, Göteborg University, Göteborg, Sweden

c Division of Community Health Sciences, St George's, University of London, London, United Kingdom

g Medical Microbiology, Department of Cellular and Molecular Medicine, St George's, University of London, London, United Kingdom

d Department of Pediatric Pneumology and Immunology, Charité Medical University, Berlin, Germany

f Pediatric Allergology Unit, Sandro Pertini Hospital, Rome, Italy

Reprint requests: Siv Ahrné, PhD, Applied Nutrition, PO Box 124, SE-22100 Lund, Sweden.

Supported by the European Framework Programme 5 (QLRT-2000-00538) and by an unrestricted grant from Probi AB, Lund, Sweden.

Disclosure of potential conflict of interest: C. Olsson owns stock in Probi AB. The rest of the authors have declared that they have no conflict of interest.

PII: S0091-6749(07)01767-8

doi:10.1016/j.jaci.2007.09.011

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