Neonatal gut colonization byStaphylococcus aureusstrains with certain adhesins and superantigens is negatively associated with subsequent development of atopic eczema

Abstract

Summary 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 the enterotoxin gene (egc) cluster and elastin‐binding protein is negatively associated with development of atopic eczema. Objectives To investigate (i) whether these findings could be replicated in a second birth cohort, FARMFLORA, and (ii) 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 random amplified polymorphic DNA and assessed for adhesin and superantigen gene carriage by polymerase chain reaction. Atopic eczema at 18 months of age was related to nasal and gut S. aureus colonization patterns during the first 2 months of life (well before onset of eczema). Results Staphylococcus aureus colonization 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 egc, compared with strains from children who remained healthy. Nasal colonization by S. aureus was less clearly related to subsequent eczema development. Conclusions The results precisely replicate our previous observations and may suggest that mucosal colonization by certain S. aureus strains provides immune stimulation that strengthens the epithelial barrier and counteracts the development of atopic eczema.

The exposome in atopic dermatitis

“…Infants whose gut strains of S aureus did not express the ebp gene encoding for elastin binding protein and the SElM superantigen were less likely to develop AD, although the mechanisms contributing to this remain to be elucidated. 86,87 The role of the microbiome is expanded further when helminth parasites and their relationship to AD development are considered.…”

“…Emerging data highlight that S aureus may also play a role in the gut. Infants whose gut strains of S aureus did not express the ebp gene encoding for elastin binding protein and the SElM superantigen were less likely to develop AD, although the mechanisms contributing to this remain to be elucidated 86,87…”

Updated understanding of Staphylococcus aureus in atopic dermatitis: From virulence factors to commensals and clonal complexes

“…Of note, early neonatal gut colonization with SA strains carrying egc was negatively associated with development of AD, further reinforcing the notion of a skin-gut axis in disease pathogenesis. 128,129 Cna encodes a protein that facilitates adhesion of SA to collagen. 130 Interestingly, cna-negative SA did not show a significant reduction in binding to AD skin when compared to wild-type SA, while SA negative for clumping factor (clf) A or B had significantly decreased binding to AD skin than its wild-type parent strain.…”

The power and potential of BIOMAP to elucidate host‐microbiome interplay in skin inflammatory diseases

“…164 For example, bacterial-derived short-chain fatty acids can exert anti-inflammatory or tolerance-inducing effects. 165,166 In culture-based studies, 167,168 early gut colonization with particular Staphylococcus aureus strains was negatively associated with later development of AD. The metabolic impact and immunologic consequences of the skin microbiome in early life, and the relationship…”