Background/Aims: The mode of delivery (vaginal or cesarean section) and feeding type (breastfeeding or formula feeding) of neonates are considered the most influential factors in the development of gut microbiota. Objectives: This study investigated the effect of prebiotic-rich breast milk on overcoming gut microbiota dysbiosis. Method: Stool samples from 36 healthy Japanese neonates were obtained at 4 days and 1 month of age, and divided into 4 groups based on mode of delivery and feeding type. The gut microbiota composition and bacterial diversity were assessed using 16S rRNA sequencing. Results: At 4 days old, vaginally delivered neonates had a significantly higher diversity of bacteria than those born by cesarean section. Bacteroidales and Enterobacteriales were overrepresented in vaginally delivered neonates (p = 0.0031 and p = 0.011), while Bacillales and Lactobacillales were overrepresented in caesarean section delivered neonates (p = 0.012 and p = 0.0016). However, there was little difference in bacterial diversity and bacterial relative abundance at 1 month of age between groups. Conclusions: Cesarean section delivery appeared to reduce the diversity of neonate gut microbiota, resulting in dysbiosis, but this improved to the equivalent level seen in vaginally delivered infants by 1 month of age. Breastfeeding, even for short periods, may therefore improve neonate gut dysbiosis.

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An IgG-induced neutrophil activation pathway contributes to human drug-induced anaphylaxis. Sci Transl Med 2019;11(500):eaat1479. 5. Francis A, Bosio E, Stone SF, et al. Markers involved in innate immunity and neutrophil activation are elevated during acute human anaphylaxis: validation of a microarray study.

The etiology of KD has been studied comprehensively but remains largely unknown. The disease seems to result from the interplay of genetic and environmental susceptibility factors with infectious triggers, followed by a subsequent abnormal immune response characterized by increased levels of inflammatory cytokines and chemokines during the acute phase. Evidence has mounted to suggest that an imbalance between T helper 17 cells (Th17s) and regulatory T cells (Tregs) is associated with aberrant immune responses in KD. Recent advances in culture-independent techniques for detection and identification of intestinal commensal bacteria enabled the discovery that Th17 and Treg differentiation are regulated by short chain fatty acids (SCFAs), in particular butyrate, produced by the gut microbiota. This finding provided a mechanistic link between dysbiosis, defined as changes in the composition of the gut microbiota, and various inflammatory diseases. On this basis, we propose that dysbiosis, with reduced production of SCFAs leading to imbalances of Th17s/Tregs, could be involved in the etiology of KD. A pilot study supported this hypothesis, as only fecal concentrations of butyrate were significantly reduced in KD patients among SCFAs. This evolving perspective prompted us to undertake metagenomic analyses of bacterial DNA from the feces of KD patients who were antibiotic-naïve at diagnosis. Simultaneous measurements of Th17s/Tregs in peripheral blood and SCFA concentrations in feces would provide valuable information regarding the association between dysbiosis and dysregulated immune responses in KD.

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