Evaluation of stool microbiota signatures in two cohorts of Asian (Singapore and Indonesia) newborns at risk of atopy

Longitudinal analysis showed associations of geographical origin with Clostridium leptum, Atopobium and Bifidobacterium groups. Mode of delivery had the largest effect on stool microbiota signatures influencing the abundance of four bacterial groups. Significantly higher abundance of bacterial members belonging to the Bacteroides-Prevotella, Bifidobacterium and Atopobium groups, but lower abundance of Lactobacilli-Enterococci group members, were observed in vaginal delivered compared to caesarean delivered infants. Demographic factors influencing the structure of infants stool microbiota during the first year of life included breastfeeding, age of weaning, sibship size and exposure to antibiotics.Differences in stool microbiota signatures were observed in relation to various demographic factors. These features may confound studies relating to the association of the structure of fecal microbiota and the predisposition to human modern disease.The human gut microbiome is a complex ecosystem harbouring a rich diversity of commensal microorganisms. It is widely thought that the early life development of the neonatal intestinal microbiota plays an important role in the maturation of the host immune system and could in turn influence allergy development [1-3]. For example, germfree mice which lack the endemic intestinal microbiota showed impairment of intestinal mucosal and systemic immune system development. The impairment in the systemic immune system is reflected by poorly formed spleen and lymph nodes, hypoplastic Peyer's patches, reduced levels of secreted IgA and IgG, and lack of expansion of CD4+ T cell populations [2,3]. Furthermore, these mice exhibited cytokine profiles that skewed towards Th2 [2], which is involved in the pathophysiology of allergic diseases.Past studies have further reported that intestinal microbiota in subjects with allergy, particularly those with atopic eczema, differed from those of healthy controls [4-7]. Wang and colleagues showed that t