Abstract

The rapid rise of atopic diseases in recent decades has increasingly turned attention to potential environmental variables that modulate allergic phenotype expression. Recent discoveries regarding the human microbiome’s complex signaling with our immune system are driving research to comprehend how altered infant microflora may result in persistently impaired immunomodulation. This systematic review and meta-analysis of published data between 2005 and 2016 seeks to clarify the evidence for a relationship between infant microbiota diversity and the development of atopic disease in later childhood. Studies were selected that analyzed the nature of the infant intestinal microbiota and the relationship to childhood atopy. Focus was directed towards studies assessing microbiota diversity although this was frequently not the primary focus of the individual papers. Selection of studies required diversity analysis calculated by non-culture methods. Exclusion of studies occurred if the assessment of children’s microflora occurred after 12 months of age, where a clinical intervention was uncontrolled or if there was a lack of clear diagnosis by laboratory or clinical methods. Twelve studies met the criteria for final inclusion with eleven used within the meta-analysis. Within the 11 studies, there are 24 effect sizes. There is a spectrum of infant ages and allergic disease within the studies including atopic dermatitis, asthma/wheeze, and food sensitisation. Infants in the control group had higher diversity scores than infants in the atopic group, d = 0.4217, 95%CI = 0.1874 to 0.6559, P = .0004. There is a significant trend within the data for early infancy as the most influential time for decreased microbiome diversity and an association with later atopy. Public health implications thus arising include reduction of unnecessary antimicrobial interventions, environmental modifications that improve healthy diversity exposure, and further research into appropriate microbial signaling to foster balanced immune responses in utero and early infancy.

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