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The results showed that reduced oxygen levels in the small intestine of neonatal rats induced by <jats:italic>Saccharomyces boulardii<\/jats:italic> accelerated microbiome colonization and type 3 immunity development, which protected against <jats:italic>Salmonella enterica<\/jats:italic> serovar Typhimurium infection. Microbiome maturation increased the abundance of microbiome\u2010encoded bile salt hydrolase (<jats:italic>BSH<\/jats:italic>) genes and hyocholic acid (HCA) levels. Furthermore, reducing oxygen levels in the intestine increased the abundance of <jats:italic>Limosilactobacillus reuteri<\/jats:italic>, a bacterium encoding <jats:italic>BSH<\/jats:italic>, and promoted intestinal type 3 immunity. However, inhibition of BSH blocked the <jats:italic>L. reuteri\u2010<\/jats:italic>induced development of intestinal type 3 immunity. Mechanistically, HCA promoted the development of gamma\u2010delta T cells and type 3 innate lymphoid cells by stabilizing the mRNA expression of RAR\u2010related orphan receptor C via the farnesoid X receptor\u2013WT1\u2010associated protein\u2010N6\u2010methyl\u2010adenosine axis. These results reveal that gut microbiota\u2010derived HCA plays a crucial role in promoting the development of intestinal type 3 immunity in neonates. 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