Neonatal gut colonisation by Staphylococcus aureus strains with certain adhesins and superantigens is negatively associated with subsequent development of atopic eczema

Abstract

Background

Insufficient early immune stimulation may predispose to atopic disease. Staphylococcus aureus, a skin and gut colonizer, produces the B‐cell mitogen protein A and T‐cell activating superantigens. Early gut colonization by S. aureus strains that possess the superantigens encoded by enterotoxin gene (egc) cluster and the elastin‐binding protein, is negatively associated with development of atopic eczema.

Objectives

To investigate whether these findings could be replicated in a second birth‐cohort, FARMFLORA and, secondly, whether nasal colonization by S. aureus also relates to subsequent atopic eczema development.

Methods

Faecal samples and nasal swabs from infants in the FARMFLORA birth‐cohort (N=65) were cultured for S. aureus. Individual strains were distinguished by RAPD (random amplified polymorphic DNA) and assessed for adhesin and superantigen gene carriage by PCR. Atopic eczema at 18 months of age was related to nasal and gut S. aureus colonisation patterns during the first 2 months of life (well before onset of eczema).

Results

S. aureus colonisation per se was unrelated to subsequent eczema development. However, gut S. aureus strains from the infants who subsequently developed atopic eczema less frequently carried the ebp gene, encoding elastin‐binding protein, and superantigen genes encoded by the egc, as compared to strains from children who remained healthy. Nasal colonization by S. aureus was less clearly related to subsequent eczema development.

Conclusion

The results precisely replicate our previous observations and may suggest that mucosal colonisation by certain S. aureus strains provides immune stimulation that strengthens the epithelial barrier and counteracts the development of atopic eczema.

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